Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. During apoptosis, cells exhibit characteristic changes such as blebbing, shrinkage, nuclear fragmentation, and chromosomal DNA fragmentation. Between 50-70 billion cells die each day in the human body through apoptosis. Apoptosis is important for development and shaping of embryos, as well as for destroying infected, cancerous, or damaged cells. Caspases are a family of cysteine proteases that play essential roles in apoptosis. There are intrinsic and extrinsic pathways of caspase activation - the intrinsic pathway involves mitochondria and the extrinsic involves death receptors. Inhibitor of apoptosis proteins can block apoptosis and lead to conditions like cancer if unregulated.
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis and necrosis are two types of cell death. Apoptosis is a regulated process where cells actively cause their own death, minimizing harm to surrounding cells and tissue. It occurs normally during development and to remove damaged cells, and is controlled through caspase activation via intrinsic and extrinsic pathways. In contrast, necrosis is unregulated cell death caused by external factors like toxins or trauma. Apoptosis plays important roles in development, tissue homeostasis, and diseases like cancer when its regulation is disrupted. The cell cycle and checkpoints also interact with apoptosis to control cell proliferation and death.
Apoptosis, or programmed cell death, is an important physiological process that eliminates unwanted or damaged cells. There are two main pathways that trigger apoptosis - the extrinsic or death receptor pathway, and the intrinsic or mitochondrial pathway. The extrinsic pathway involves death receptors and ligands that activate caspase enzymes. The intrinsic pathway occurs in response to cellular stress and involves mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. This forms the apoptosome complex and activates caspase-9 and caspase-3, leading to apoptosis. Apoptosis is a highly regulated process involving Bcl-2 family proteins, caspase enzymes, and characteristic morphological changes including cell shrinkage, nuclear fragmentation, and membrane blebbing. Assays to detect
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. During apoptosis, cells exhibit characteristic changes such as blebbing, shrinkage, nuclear fragmentation, and chromosomal DNA fragmentation. Between 50-70 billion cells die each day in the human body through apoptosis. Apoptosis is important for development and shaping of embryos, as well as for destroying infected, cancerous, or damaged cells. Caspases are a family of cysteine proteases that play essential roles in apoptosis. There are intrinsic and extrinsic pathways of caspase activation - the intrinsic pathway involves mitochondria and the extrinsic involves death receptors. Inhibitor of apoptosis proteins can block apoptosis and lead to conditions like cancer if unregulated.
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
Hi! I am Komal Sankaran, M.Sc. Biotechnology (Pune University Gold Medalist, 2013), CSIR-NET SPM fellow (Jun- 2014, 4th rank), CSIR-NET- LS (Dec 2013, 2nd rank), DBT JRF category- I. Please contact if anyone is interested in Life Sciences CSIR-NET coaching in Pune (Khadki area).
Email- komalsan91@gmail.com
Apoptosis and necrosis are two types of cell death. Apoptosis is a regulated process where cells actively cause their own death, minimizing harm to surrounding cells and tissue. It occurs normally during development and to remove damaged cells, and is controlled through caspase activation via intrinsic and extrinsic pathways. In contrast, necrosis is unregulated cell death caused by external factors like toxins or trauma. Apoptosis plays important roles in development, tissue homeostasis, and diseases like cancer when its regulation is disrupted. The cell cycle and checkpoints also interact with apoptosis to control cell proliferation and death.
Apoptosis, or programmed cell death, is an important physiological process that eliminates unwanted or damaged cells. There are two main pathways that trigger apoptosis - the extrinsic or death receptor pathway, and the intrinsic or mitochondrial pathway. The extrinsic pathway involves death receptors and ligands that activate caspase enzymes. The intrinsic pathway occurs in response to cellular stress and involves mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. This forms the apoptosome complex and activates caspase-9 and caspase-3, leading to apoptosis. Apoptosis is a highly regulated process involving Bcl-2 family proteins, caspase enzymes, and characteristic morphological changes including cell shrinkage, nuclear fragmentation, and membrane blebbing. Assays to detect
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
Three studies on programmed cell death in plants are summarized:
1. A study showed that heat-induced cell death in cucumber cotyledons resulted in DNA fragmentation and the release of cytochrome c from mitochondria into the cytosol, demonstrating conserved mechanisms with animal apoptosis.
2. A study found that caspase-specific peptide inhibitors effectively inhibited chemically-induced cell death in tomato cells, indicating caspase-like proteases mediate plant apoptotic pathways.
3. A study showed that anthocyanins from black soybeans protected human skin cells from UVB-induced reactive oxygen species, apoptosis, and caspase activation by preventing pro-apoptotic signaling.
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
The document summarizes key aspects of apoptosis including:
- The origins and definition of the term apoptosis from Greek meaning "falling leaves".
- The significance of apoptosis in development and maintenance of tissues by removing excess or damaged cells.
- The morphological features of apoptosis including membrane blebbing, nuclear fragmentation, and formation of apoptotic bodies.
- The molecular mechanisms including caspase signaling pathways like the intrinsic pathway involving mitochondria and the extrinsic pathway involving death receptors.
- Regulatory mechanisms involving proteins like Bcl-2 that balance survival and death signals.
- Dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and HIV infection.
Apoptosis is a programmed cell death process that removes unwanted cells. It is mediated by caspase enzymes and leads to cell fragmentation into apoptotic bodies that are phagocytosed. There are two main pathways - the intrinsic mitochondrial pathway, where cellular stress leads to mitochondrial cytochrome c release and caspase activation, and the extrinsic death receptor pathway, where death ligands such as FasL bind receptors and recruit caspase-8. Both pathways activate executioner caspases like caspase-3 to degrade cellular proteins and carry out apoptosis. Disorders can arise from too little apoptosis, allowing abnormal cell survival like in cancer, or excessive apoptosis leading to cell loss in diseases like neurodegeneration.
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
The document summarizes key aspects of cell cycle regulation in plants. It discusses the cell cycle phases of interphase (G1, S, G2) and mitosis. Key regulators of the plant cell cycle include cyclin-dependent kinases (CDKs) and cyclins. CDKs activate during specific cell cycle phases upon binding to cyclins. Plant hormones also influence the cell cycle through effects on CDKs, cyclins and other regulators. Precise control of the cell cycle is important for plant growth and development.
iPSCs are pluripotent; unlike ESC, iPSCs are not derived from the embryo, but instead created from differentiated cells in the lab through a process – cellular reprogramming.
The document provides an overview of apoptosis, or programmed cell death, discussing its molecular mechanisms and role in development and disease. It summarizes that apoptosis occurs through intrinsic and extrinsic pathways, is regulated by Bcl-2 family proteins like Bax and Bcl-2, and involves caspase activation leading to DNA fragmentation and phagocytosis of cell fragments. The document also discusses the importance of apoptosis in immune system development and its relevance to cancer.
This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
Apoptosis is a tightly regulated form of programmed cell death that plays an important role in tissue homeostasis, development, and the immune system. It is characterized by fragmentation of DNA and the nucleus. There are two main pathways that trigger apoptosis - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway - which both activate caspases and lead to dismantling of the cell. Apoptosis is important for removing damaged, unneeded, or infected cells, and balancing it with cell proliferation is critical for health.
Apoptosis, or programmed cell death, is an internally controlled suicide program where cells are removed with minimal disruption of surrounding tissue. It plays important roles in development, tissue homeostasis, and defense against infection and cancer. There are two main apoptotic pathways - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. Both pathways activate caspases, cysteine proteases that cleave proteins to execute the cell death program through processes like DNA fragmentation and formation of apoptotic bodies. Deregulation of apoptosis contributes to cancer development by allowing damaged or unnecessary cells to survive. Targeting the apoptotic pathway is a strategy for cancer treatment.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
Apoptosis is a tightly regulated form of programmed cell death that is controlled by specific genes. During apoptosis, cells fragment their DNA and nuclei and form apoptotic bodies that are phagocytosed by other cells without causing inflammation. This process removes damaged or unnecessary cells in a controlled manner. Apoptosis can be triggered by physiologic processes like development or pathologic conditions like radiation, viral infections, or accumulation of misfolded proteins. It occurs through either the intrinsic mitochondrial pathway involving cytochrome c release or the extrinsic death receptor pathway. Precise genetic control of apoptosis is important for tissue homeostasis and manipulation of these pathways may help treat diseases like cancer.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
Every cell has a natural life cycle involving birth and death. There are two main types of cell death: necrosis and apoptosis. Necrosis is accidental cell death due to external injury, while apoptosis is a carefully regulated process in which cells play an active role in their own death. During apoptosis, cells shrink, break into fragments, and are phagocytosed without causing inflammation. Precisely regulated apoptosis is important for normal development, immune function, and homeostasis, while defects can lead to diseases. Many cancer therapies aim to trigger the apoptosis pathway in tumor cells.
1. Apoptosis is a tightly regulated form of programmed cell death that plays an important role in development, tissue homeostasis, and the immune system. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
2. The process of apoptosis involves initiator caspases that activate executioner caspases, leading to degradation of nuclear and cytoplasmic components. Mitochondria also play a key role by releasing pro-apoptotic factors. Various proteins regulate apoptosis, including Bcl-2 family members and inhibitors of apoptosis (IAPs).
3. Dysregulation of apoptosis contributes to diseases like cancer, neurodegeneration, and HIV/AIDS. Detection of
1. Programmed cell death (PCD) refers to regulated cell death processes that eliminate cells when they are no longer useful or potentially harmful.
2. Apoptosis is a form of PCD characterized by nuclear fragmentation, chromatin condensation, cell shrinkage and blebbing, and formation of apoptotic bodies that are quickly phagocytosed, avoiding inflammation. It relies on caspase activation through the mitochondrial or death receptor pathways.
3. Alternative cell death pathways include necroptosis, pyroptosis and autophagy. Necroptosis resembles necrosis morphologically but is caspase-independent and regulated. Pyroptosis involves caspase-1 and occurs during microbial infection, triggering inflammation. Autophagy
1. Programmed cell death, also known as apoptosis, is essential for proper development and for destroying harmful cells.
2. Apoptosis is regulated by caspases, which are cysteine-dependent aspartate specific proteases. Caspases activate a proteolytic cascade that leads to cell death.
3. There are three main apoptotic pathways: the extrinsic pathway which involves death receptors, the intrinsic pathway which involves the mitochondria, and the granzyme pathway which uses granzymes from cytotoxic T cells and natural killer cells.
Apoptosis - programmed cell death that occurs in multicellular organismsMeethuRappai1
This document defines apoptosis and describes the intrinsic and extrinsic pathways that regulate programmed cell death. Apoptosis is characterized by activation of enzymes that degrade a cell's nuclear DNA and proteins. It can be triggered through intrinsic signals like DNA damage or extrinsic factors like death receptors. Both pathways activate caspases that execute apoptosis. Phagocytosis efficiently removes apoptotic cells to prevent inflammation. Dysregulation of apoptosis can cause cancer if cells survive too long or neurodegenerative diseases if excessive cell death occurs.
This document provides an overview of apoptosis, or programmed cell death. It begins with an introduction defining apoptosis and its importance in development, aging, and disease. It then describes the main types and mechanisms of apoptosis, including the extrinsic and intrinsic pathways. Key features of apoptosis like morphology, assays to detect it, and differences from necrosis are summarized. The document concludes by discussing other forms of programmed cell death and clinical applications of understanding apoptosis.
Apoptosis is a controlled, programmed cell death process that is essential for normal development and homeostasis. During apoptosis, cells actively trigger intracellular events that lead to cell fragmentation and phagocytosis without causing inflammation. Apoptosis is distinct from necrosis, which is unregulated cell death caused by external cellular injuries. Key aspects of apoptosis include activation of caspases, DNA fragmentation, and changes to cell membranes that mark cells for phagocytosis. Apoptosis pathways can be triggered by extracellular signals or internal cell damage and are important in development, tissue homeostasis, and diseases like cancer when the process goes awry.
Three studies on programmed cell death in plants are summarized:
1. A study showed that heat-induced cell death in cucumber cotyledons resulted in DNA fragmentation and the release of cytochrome c from mitochondria into the cytosol, demonstrating conserved mechanisms with animal apoptosis.
2. A study found that caspase-specific peptide inhibitors effectively inhibited chemically-induced cell death in tomato cells, indicating caspase-like proteases mediate plant apoptotic pathways.
3. A study showed that anthocyanins from black soybeans protected human skin cells from UVB-induced reactive oxygen species, apoptosis, and caspase activation by preventing pro-apoptotic signaling.
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
The document summarizes key aspects of apoptosis including:
- The origins and definition of the term apoptosis from Greek meaning "falling leaves".
- The significance of apoptosis in development and maintenance of tissues by removing excess or damaged cells.
- The morphological features of apoptosis including membrane blebbing, nuclear fragmentation, and formation of apoptotic bodies.
- The molecular mechanisms including caspase signaling pathways like the intrinsic pathway involving mitochondria and the extrinsic pathway involving death receptors.
- Regulatory mechanisms involving proteins like Bcl-2 that balance survival and death signals.
- Dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and HIV infection.
Apoptosis is a programmed cell death process that removes unwanted cells. It is mediated by caspase enzymes and leads to cell fragmentation into apoptotic bodies that are phagocytosed. There are two main pathways - the intrinsic mitochondrial pathway, where cellular stress leads to mitochondrial cytochrome c release and caspase activation, and the extrinsic death receptor pathway, where death ligands such as FasL bind receptors and recruit caspase-8. Both pathways activate executioner caspases like caspase-3 to degrade cellular proteins and carry out apoptosis. Disorders can arise from too little apoptosis, allowing abnormal cell survival like in cancer, or excessive apoptosis leading to cell loss in diseases like neurodegeneration.
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
The document summarizes key aspects of cell cycle regulation in plants. It discusses the cell cycle phases of interphase (G1, S, G2) and mitosis. Key regulators of the plant cell cycle include cyclin-dependent kinases (CDKs) and cyclins. CDKs activate during specific cell cycle phases upon binding to cyclins. Plant hormones also influence the cell cycle through effects on CDKs, cyclins and other regulators. Precise control of the cell cycle is important for plant growth and development.
iPSCs are pluripotent; unlike ESC, iPSCs are not derived from the embryo, but instead created from differentiated cells in the lab through a process – cellular reprogramming.
The document provides an overview of apoptosis, or programmed cell death, discussing its molecular mechanisms and role in development and disease. It summarizes that apoptosis occurs through intrinsic and extrinsic pathways, is regulated by Bcl-2 family proteins like Bax and Bcl-2, and involves caspase activation leading to DNA fragmentation and phagocytosis of cell fragments. The document also discusses the importance of apoptosis in immune system development and its relevance to cancer.
This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
Apoptosis is a tightly regulated form of programmed cell death that plays an important role in tissue homeostasis, development, and the immune system. It is characterized by fragmentation of DNA and the nucleus. There are two main pathways that trigger apoptosis - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway - which both activate caspases and lead to dismantling of the cell. Apoptosis is important for removing damaged, unneeded, or infected cells, and balancing it with cell proliferation is critical for health.
Apoptosis, or programmed cell death, is an internally controlled suicide program where cells are removed with minimal disruption of surrounding tissue. It plays important roles in development, tissue homeostasis, and defense against infection and cancer. There are two main apoptotic pathways - the intrinsic mitochondrial pathway and the extrinsic death receptor pathway. Both pathways activate caspases, cysteine proteases that cleave proteins to execute the cell death program through processes like DNA fragmentation and formation of apoptotic bodies. Deregulation of apoptosis contributes to cancer development by allowing damaged or unnecessary cells to survive. Targeting the apoptotic pathway is a strategy for cancer treatment.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
Apoptosis is a tightly regulated form of programmed cell death that is controlled by specific genes. During apoptosis, cells fragment their DNA and nuclei and form apoptotic bodies that are phagocytosed by other cells without causing inflammation. This process removes damaged or unnecessary cells in a controlled manner. Apoptosis can be triggered by physiologic processes like development or pathologic conditions like radiation, viral infections, or accumulation of misfolded proteins. It occurs through either the intrinsic mitochondrial pathway involving cytochrome c release or the extrinsic death receptor pathway. Precise genetic control of apoptosis is important for tissue homeostasis and manipulation of these pathways may help treat diseases like cancer.
here is some information about autophagy, how it happend, when it happend and it's mechanism.
and some information about it's effect on cancer and some disorders.
Every cell has a natural life cycle involving birth and death. There are two main types of cell death: necrosis and apoptosis. Necrosis is accidental cell death due to external injury, while apoptosis is a carefully regulated process in which cells play an active role in their own death. During apoptosis, cells shrink, break into fragments, and are phagocytosed without causing inflammation. Precisely regulated apoptosis is important for normal development, immune function, and homeostasis, while defects can lead to diseases. Many cancer therapies aim to trigger the apoptosis pathway in tumor cells.
1. Apoptosis is a tightly regulated form of programmed cell death that plays an important role in development, tissue homeostasis, and the immune system. It is characterized by morphological changes including cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
2. The process of apoptosis involves initiator caspases that activate executioner caspases, leading to degradation of nuclear and cytoplasmic components. Mitochondria also play a key role by releasing pro-apoptotic factors. Various proteins regulate apoptosis, including Bcl-2 family members and inhibitors of apoptosis (IAPs).
3. Dysregulation of apoptosis contributes to diseases like cancer, neurodegeneration, and HIV/AIDS. Detection of
1. Programmed cell death (PCD) refers to regulated cell death processes that eliminate cells when they are no longer useful or potentially harmful.
2. Apoptosis is a form of PCD characterized by nuclear fragmentation, chromatin condensation, cell shrinkage and blebbing, and formation of apoptotic bodies that are quickly phagocytosed, avoiding inflammation. It relies on caspase activation through the mitochondrial or death receptor pathways.
3. Alternative cell death pathways include necroptosis, pyroptosis and autophagy. Necroptosis resembles necrosis morphologically but is caspase-independent and regulated. Pyroptosis involves caspase-1 and occurs during microbial infection, triggering inflammation. Autophagy
1. Programmed cell death, also known as apoptosis, is essential for proper development and for destroying harmful cells.
2. Apoptosis is regulated by caspases, which are cysteine-dependent aspartate specific proteases. Caspases activate a proteolytic cascade that leads to cell death.
3. There are three main apoptotic pathways: the extrinsic pathway which involves death receptors, the intrinsic pathway which involves the mitochondria, and the granzyme pathway which uses granzymes from cytotoxic T cells and natural killer cells.
Apoptosis - programmed cell death that occurs in multicellular organismsMeethuRappai1
This document defines apoptosis and describes the intrinsic and extrinsic pathways that regulate programmed cell death. Apoptosis is characterized by activation of enzymes that degrade a cell's nuclear DNA and proteins. It can be triggered through intrinsic signals like DNA damage or extrinsic factors like death receptors. Both pathways activate caspases that execute apoptosis. Phagocytosis efficiently removes apoptotic cells to prevent inflammation. Dysregulation of apoptosis can cause cancer if cells survive too long or neurodegenerative diseases if excessive cell death occurs.
This document provides an overview of apoptosis, or programmed cell death. It begins with an introduction defining apoptosis and its importance in development, aging, and disease. It then describes the main types and mechanisms of apoptosis, including the extrinsic and intrinsic pathways. Key features of apoptosis like morphology, assays to detect it, and differences from necrosis are summarized. The document concludes by discussing other forms of programmed cell death and clinical applications of understanding apoptosis.
The document provides an overview of apoptosis, or programmed cell death. It describes the three main pathways that can trigger apoptosis: the extrinsic or death receptor pathway, the intrinsic or mitochondrial pathway, and the perforin/granzyme pathway. The pathways activate initiator caspases that go on to activate executioner caspases, leading to characteristic cell changes like nuclear fragmentation and membrane blebbing. Apoptotic cells are then phagocytosed to prevent inflammation.
physiology of apoptosis first year mbbs medical.pdfDratoshKatiyar
The document summarizes apoptosis (programmed cell death) through three parts:
Part 1 introduces apoptosis, its history, morphological hallmarks, and provides examples of apoptosis in development including web-footed chickens.
Part 2 describes the key mechanisms and pathways of apoptosis including caspases, the intrinsic mitochondrial pathway involving Bcl-2 proteins and p53, and the extrinsic death receptor pathway.
Part 3 outlines the importance of apoptosis in normal physiology and development and consequences of deregulated apoptosis such as neurodegeneration when in excess and cancer when deficient.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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Apoptosis is a
-pathway of cell death that is
-induced by an internally regulated program
-in which cells destined to die activate intrinsic enzymes that --degrade the cells’ own nuclear DNA and also nuclear and cytoplasmic proteins
-With minimal host reaction.
Apoptosis is a form of programmed cell death that is mediated by activation of caspases. It plays an important role in both physiological processes like development and pathological conditions like DNA damage. The key features of apoptosis include cell shrinkage, chromatin condensation, formation of apoptotic bodies, and phagocytosis of cell fragments without eliciting inflammation. The intrinsic and extrinsic pathways initiate apoptosis through an imbalance of survival and death signals within cells.
Add MTT reagent and incubate. Mitochondrial enzymes in viable cells convert MTT into an insoluble purple formazan product. Lyse cells and solubilize formazan with solvent. Measure absorbance which is directly proportional to number of viable cells. The more viable cells, the higher the absorbance. MTT assay is a sensitive, quantitative and reliable colorimetric method to measure cell viability and proliferation.
Intrinsic and Extrinsic Pathway of ApoptosisAnantha Kumar
This document provides an overview of apoptosis (programmed cell death) at the cellular level. It discusses how apoptosis can be initiated through either the intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell like mitochondrial membrane permeability, while the extrinsic pathway involves death receptors on the cell surface and their ligands. Key proteins and complexes involved in each pathway are caspase enzymes and the apoptosome. Research on apoptosis has increased understanding of diseases like cancer that involve deregulated cell proliferation and death.
Apoptosis is a programmed cell death process that occurs in multicellular organisms. It is characterized by cell shrinkage, nuclear fragmentation, and global mRNA decay. Apoptosis ensures the orderly disposal of cells and occurs during normal cell turnover, development, and aging. It also helps remove infected, damaged or unnecessary cells. There are two main pathways of apoptosis - the intrinsic pathway which is triggered by intracellular signals within the cell, and the extrinsic pathway which is initiated by activation of cell surface death receptors by extracellular ligands. Both pathways activate caspases, a family of cysteine proteases, that trigger the degradation of proteins and DNA fragmentation that leads to cell death. Deregulation of apoptosis can contribute to diseases like cancer
There are 4 main pathways of programmed cell death or apoptosis: 1) the extrinsic or death receptor pathway, 2) the intrinsic or mitochondrial pathway, 3) the perforin pathway, and 4) the execution pathway. The extrinsic pathway involves death receptors and ligands that form a death-inducing signaling complex leading to caspase activation. The intrinsic pathway involves mitochondrial membrane changes releasing proteins like cytochrome c that activate caspases via apoptosomes. The perforin pathway uses granzymes from cytotoxic cells to directly or indirectly activate caspases. Both pathways activate caspase-3 in the execution phase, which degrades nuclear material and proteins to dismantle the cell.
This document provides an overview of apoptosis in health and disease. It begins with definitions of apoptosis and its key characteristics. It then discusses the intrinsic and extrinsic pathways of apoptosis, involving proteins like caspases, Bcl-2 family members, cytochrome c, and death receptors. The document outlines the morphological changes seen in apoptotic cells and methods to detect apoptosis. It discusses the significance of apoptosis in physiological conditions like development and tissue homeostasis. Finally, it examines how dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and neurodegenerative conditions.
Apoptosis, or programmed cell death, is a vital process in the body that occurs through development, aging, and when cells are damaged. It is characterized by distinct morphological changes and biochemical mechanisms. The process involves caspase activation and a complex cascade of events. There are three main pathways that trigger apoptosis - the intrinsic pathway which involves mitochondria, the extrinsic or death receptor pathway activated by extracellular signals, and the perforin/granzyme pathway used by cytotoxic T cells. All pathways ultimately activate executioner caspases like caspase-3 to carry out the final stages of apoptosis.
Programmed cell death, also known as apoptosis, is a naturally occurring process where a cell is directed to die in a controlled manner. During apoptosis, cells shrink and break into fragments that are easily removed by phagocytes without causing inflammation. This process is important for tissue homeostasis, development, the immune system, and removal of damaged cells. Apoptosis is characterized by specific morphological changes like blebbing, nuclear fragmentation, chromatin condensation, and formation of apoptotic bodies. Understanding apoptosis provides insights into cancer development and potential new treatments.
The document discusses apoptosis, or programmed cell death. It describes the intrinsic and extrinsic pathways of apoptosis, as well as the morphological changes that occur during apoptosis, including cell shrinkage, organelle reduction, mitochondrial leakage, chromatin condensation, nuclear fragmentation, and membrane blebbing. Apoptosis is an important process for development and maintenance of healthy tissues by removing damaged or unneeded cells.
Apoptosis is a tightly regulated and programmed form of cell death that is essential for tissue homeostasis. It is characterized by nuclear fragmentation, membrane blebbing, and phagocytosis of cellular debris without inflammation. The intrinsic pathway is mediated by mitochondria and pro-apoptotic Bcl-2 family proteins, while the extrinsic pathway involves death receptors and caspase activation. Caspases are cysteine proteases that dismantle the cell through cleavage of structural proteins and DNA. Apoptosis must be balanced, as too little can lead to cancer and too much can contribute to diseases.
The document summarizes different types of cell death including programmed cell death (PCD), apoptosis, necrosis, and autophagy. It describes key aspects of apoptosis such as the intrinsic and extrinsic pathways, the role of caspases and Bcl-2 proteins, mitochondrial involvement, and morphological changes cells undergo during apoptosis. Necrosis is described as unprogrammed cell death caused by external factors like trauma or infection. Autophagy is noted as another form of programmed cell death.
1) Cell death occurs through two main mechanisms: necrosis and apoptosis.
2) Apoptosis is a regulated process of cell death where the cell degrades its own DNA and proteins, keeping the plasma membrane intact. Apoptotic bodies are then cleared by phagocytes without causing inflammation.
3) Apoptosis is triggered through either the intrinsic mitochondrial pathway, involving cytochrome c release from mitochondria, or the extrinsic death receptor pathway, involving death ligands binding to cell surface receptors. Both pathways activate caspases to degrade the cell.
Similar to Apoptosis definition, mechanism , Apoptosis vs necrosis, Assays of apoptosis, and diseases related to Apoptosis (20)
Remote Sensing and Computational, Evolutionary, Supercomputing, and Intellige...University of Maribor
Slides from talk:
Aleš Zamuda: Remote Sensing and Computational, Evolutionary, Supercomputing, and Intelligent Systems.
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Inter-Society Networking Panel GRSS/MTT-S/CIS Panel Session: Promoting Connection and Cooperation
https://www.etran.rs/2024/en/home-english/
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...Leonel Morgado
Current descriptions of immersive learning cases are often difficult or impossible to compare. This is due to a myriad of different options on what details to include, which aspects are relevant, and on the descriptive approaches employed. Also, these aspects often combine very specific details with more general guidelines or indicate intents and rationales without clarifying their implementation. In this paper we provide a method to describe immersive learning cases that is structured to enable comparisons, yet flexible enough to allow researchers and practitioners to decide which aspects to include. This method leverages a taxonomy that classifies educational aspects at three levels (uses, practices, and strategies) and then utilizes two frameworks, the Immersive Learning Brain and the Immersion Cube, to enable a structured description and interpretation of immersive learning cases. The method is then demonstrated on a published immersive learning case on training for wind turbine maintenance using virtual reality. Applying the method results in a structured artifact, the Immersive Learning Case Sheet, that tags the case with its proximal uses, practices, and strategies, and refines the free text case description to ensure that matching details are included. This contribution is thus a case description method in support of future comparative research of immersive learning cases. We then discuss how the resulting description and interpretation can be leveraged to change immersion learning cases, by enriching them (considering low-effort changes or additions) or innovating (exploring more challenging avenues of transformation). The method holds significant promise to support better-grounded research in immersive learning.
ESR spectroscopy in liquid food and beverages.pptxPRIYANKA PATEL
With increasing population, people need to rely on packaged food stuffs. Packaging of food materials requires the preservation of food. There are various methods for the treatment of food to preserve them and irradiation treatment of food is one of them. It is the most common and the most harmless method for the food preservation as it does not alter the necessary micronutrients of food materials. Although irradiated food doesn’t cause any harm to the human health but still the quality assessment of food is required to provide consumers with necessary information about the food. ESR spectroscopy is the most sophisticated way to investigate the quality of the food and the free radicals induced during the processing of the food. ESR spin trapping technique is useful for the detection of highly unstable radicals in the food. The antioxidant capability of liquid food and beverages in mainly performed by spin trapping technique.
Or: Beyond linear.
Abstract: Equivariant neural networks are neural networks that incorporate symmetries. The nonlinear activation functions in these networks result in interesting nonlinear equivariant maps between simple representations, and motivate the key player of this talk: piecewise linear representation theory.
Disclaimer: No one is perfect, so please mind that there might be mistakes and typos.
dtubbenhauer@gmail.com
Corrected slides: dtubbenhauer.com/talks.html
The binding of cosmological structures by massless topological defectsSérgio Sacani
Assuming spherical symmetry and weak field, it is shown that if one solves the Poisson equation or the Einstein field
equations sourced by a topological defect, i.e. a singularity of a very specific form, the result is a localized gravitational
field capable of driving flat rotation (i.e. Keplerian circular orbits at a constant speed for all radii) of test masses on a thin
spherical shell without any underlying mass. Moreover, a large-scale structure which exploits this solution by assembling
concentrically a number of such topological defects can establish a flat stellar or galactic rotation curve, and can also deflect
light in the same manner as an equipotential (isothermal) sphere. Thus, the need for dark matter or modified gravity theory is
mitigated, at least in part.
When I was asked to give a companion lecture in support of ‘The Philosophy of Science’ (https://shorturl.at/4pUXz) I decided not to walk through the detail of the many methodologies in order of use. Instead, I chose to employ a long standing, and ongoing, scientific development as an exemplar. And so, I chose the ever evolving story of Thermodynamics as a scientific investigation at its best.
Conducted over a period of >200 years, Thermodynamics R&D, and application, benefitted from the highest levels of professionalism, collaboration, and technical thoroughness. New layers of application, methodology, and practice were made possible by the progressive advance of technology. In turn, this has seen measurement and modelling accuracy continually improved at a micro and macro level.
Perhaps most importantly, Thermodynamics rapidly became a primary tool in the advance of applied science/engineering/technology, spanning micro-tech, to aerospace and cosmology. I can think of no better a story to illustrate the breadth of scientific methodologies and applications at their best.
2. Table of content
Introduction
History
Morphological changes
Importance of apoptosis
Biochemical changes
Mechanism of apoptosis
Assays of apoptosis
Apoptosis in disease
Conclusion
3. Introduction
• Release of enzymes in the cell that cause the degradation of the
cells own nuclear DNA, nuclear and cytoplasmic proteins leading
to cell death.
• The word Apoptosis means “Falling of”.
• Differs from necrosis as no swelling occurs
• Plasma membrane is altered and is called apoptotic bodies.
• Apoptotic bodies being highly “edible” are consumed easily by
Phagocytes.
4. History
• Term was given by Hippocrates
• Described by Rudolf Virchow
• Defined by Kerr in 1972
• In the 20th century the research is focused for clarification of
this method to cure diseases such as cancer, Alzheimer and
AIDS.
5. Morphological changes
• Apoptosis is characterized by:
– Mitochondrial leakage
– Activation of Caspases
– Shrinkage of the cell
– Membrane bound apoptotic bodies
– Chromatin condensation
– Phagocytosis by nearby cells
6. Importance of Apoptosis
• To eliminate harmful cells and cells that have lived
their usefulness.
– During growth old cells are replaced with new ones
– Unwanted cells are eliminated to prevent inflammation
and proliferation.
– Excess leukocytes left at the end of immune response
are eliminated.
– Lymphocytes that can cause auto-immune disease are
eliminated.
7. Cont.
• Occurs when cells are damaged especially
when damage is irreparable ( DNA or proteins
are damaged)
– Damage due to radiation and cytotoxic drugs.
– Misfolded proteins cause apoptosis
– Infection due to virus or infectious agents.
8. BIOCHEMICAL CHANGES IN
APOPTOSIS
Characteristic biochemical changes in cells undergoing
apoptosis:
I. Different proteins regulate these processes
II. ATP is required
III. DNA fragmentation occurs
IV. A series of reactions of activation of proteins take place.
9. Cont.
V. pH of the cell becomes acidic
VI. The apoptosis doesn’t effect adjacent cells
VII.Very rarely it requires medical treatment and
doesn’t case inflammation.
11. Mechanism
• Apoptosis is regulated by biochemical pathways that control
the balance of death and survival inducing signals and
ultimately the activation of enzymes called Caspases.
• There are two different pathways for signaling apoptosis
– Mitochondrial Pathway (intrinsic pathway)
– Death Receptor Pathway (Extrinsic pathway)
• Both the pathways activate Caspases Proteins.
12. Intrinsic Pathway
The intrinsic apoptosis pathway is activated by a
range of exogenous and endogenous stimuli,
such as DNA damage, ischemia, and oxidative
stress.
It plays an important function in the elimination
of damaged cells.
15. Mitochondria along with
cytochrome-c also release a protein
called Smac/DIABLO.
It promote apoptosis and inhibit
anti-apoptosis proteins called
inhibitor of apoptosis proteins
(IAPs).
Cont.
16. • Entry of cytochrome-c into cytosol causes assembly of
Apoptosomes.
• Apaf-1 protein with cytochrome-c forms the seven
fold ring structure (apoptosomes)
• The attachment of caspases to the card domain of the
apoptosomes causes their activation.
Cont.
17.
18. WORKING OF CASPASE-3
Caspase-3 degraded the nuclease inhibitor and
consequently nuclease activated.
Nuclease degraded the DNA inside nucleus.
As a result cell cannot survive.
Along caspase-9, caspase-2, caspase-8 and caspase-
10 initiate apoptosis.
19. Caspase-3, caspase-6 and caspase-7 involved in
apoptosis.
Caspase-6 cause disintegration of lamina and
cytoskeleton.
P53 also activate protease for the degradation of
protein.
All these incidents leads to cell death and
phagocytosis by macrophages.
Cont.
21. Death Receptors
• “Death receptors” that are members of the tumor
necrosis factor (TNF) receptor superfamily.
• Death receptors have a cytoplasmic domain of about
80 amino acids called the “death domain”.
• This death domain plays a critical role in transmitting
the death signal from the cell surface to the
intracellular signaling pathways.
22. Death Ligand
• The best characterized receptors & ligands corresponding death
receptors include:
Ligands Receptors
• FasR (CD95/APO1) FasL
• DR3 Apo3L
• DR4 (TRAIL-R1) Apo2L
• DR5 (TRAIL-R2) Apo2L
• TNFR1 TNF-α
• TNFR2 TNF-ß
23. Apoptotic Adaptor Proteins
• Apoptotic adaptor proteins play a critical role in regulating
pro- and anti-apoptotic signaling pathways Adaptor
proteins;
• FADD (Fas-associated death domain)
• TRADD (TNF receptor-associated death domain), are
recruited to ligand-activated, oligomerized death receptors
to mediate apoptotic signaling pathways.
33. Assays of apoptosis
• Two different assay types are used to detect the
process of apoptosis
• The first assay detects initial events, whereas second
assay identifies the execution or terminal phase
• The apoptosis assays have been divided into six
different groups.
34. Cytomorphological altercation
• The observation of hematoxylin and eosin-stained tissue sections
with light microscopy allows the visualization of apoptotic cells.
• This method detects the cells in the later events of apoptosis, but
the cells in the early stage of apoptosis are not recognized.
• Transmission electron microscopy (TEM) is the gold standard for
the confirmation of apoptosis.
35. Cont.
• In TEM, cells undergoing apoptosis reveals several structural characteristics.
These characters include:
– electron-dense nucleus (marginalization of the nucleus in the early phase)
– nuclear fragmentation
– intact cell membrane even late in the cell disintegration phase
– disorganized cytoplasmic organelles
– large clear vacuoles
– phosphatidylserine at the cell surface.
• With the progression of apoptosis, these cells will lose the cell-to-cell
adhesions and will separate from neighboring cells.
• Eventually, the cell will fragment into apoptotic bodies with intact cell
membranes and will contain cytoplasmic organelles with or without nuclear
fragments.
36. DNA Fragmentation
• DNA Laddering technique can be used to detect apoptosis
– It involves the extraction of DNA from lysed cell homogenate separation by agarose gel
electrophoresis.
– The resulting bands of DNA form a DNA ladder that can be used to detect apoptosis in
tissues where the number of apoptic cells is high
– This technique can only detect apoptosis at the later stage.
• Another method include Terminal dUTP Nick end-labeling
(TUNEL).
– It detects the endonuclease cleavage products by enzymatically labelling the ends of
DNA strands.
– Terminal transferase is used to attach dUTP to the 3;-end of the DNA fragments.
– The dUTP is then labelled with variety of probes to allow detection by
light microscope, flourescence microscopy or flow cytometery.
– Although it is efficient but can give false result.
37.
38. Cont.
• Another method include Terminal dUTP Nick end-labeling
(TUNEL).
– It detects the endonuclease cleavage products by enzymatically
labelling the ends of DNA strands.
– Terminal transferase is used to attach dUTP to the 3’-end of the
DNA fragments.
– The dUTP is then labelled with variety of probes to allow
detection by light microscope, fluorescence microscopy or flow
cytometery.
– Although it is efficient but can give false result.
39.
40. Detection of Caspases
• More than 13 known caspases activity can be detected using various
types of assays.
• Immunoassays can detect cleaved substrates such as PARP and
known cell modifications such as phosphorylated histones.
• Western Blot, immunoprecipitation and immunohistochemistry
assays can be used to detect caspases activation.
• Real time PCR is also used to detect the expression of 112 genes
involved in apoptosis
• Microarrays are made to produce expression of genes that
encode factors involved in the regulation of programmed cell death.
41. Mitchondrial alterations
• Annexin V assays are used as early markers of apoptosis events.
• The translocation of phophatidylserine on the membrane surface is
an early event in apoptosis and can be detected by this assay.
• The cell is first bound to the FITC-labeled annexin V and
visualized with fluorescence microscopy.
• The integrity of membrane in apoptotic cell can also be detected
by Propidium iodide and trypan blue dyes.
• The dye may move inside the cell and then can also be visualized by
a light microscope.
43. Detection in Whole Mounts
• Whole embryo or tissue can be visualized by Acridine orange,
Nile Blue Sulfate (NBS) and Neutral Red dyes.
• All the mentioned dyes are Acidophillic and concentrate in
regions where lysosomal and phagocytic activity is high.
• Drawback of this procedure is that Acridine orange is mutagenic
and toxic. Whereas NBS and Neutral Red do not penetrate deep
into tissues and can be lost during penetration.
44. Mitochondrial assays
• Mitochondria are important cellular organelles that maintain crucial
cellular energy balance, contain key regulators of cell death processes such
as apoptosis.
• Collapse of mitochondrial membrane potential is believed to coincide with
the permeabilization of the outer mitochondrial membrane, and release of
Cytochrome C and other pro-apoptotic proteins into the cytosol, which
then triggers the downstream events in the apoptotic cascade.
• The Laser scanning confocal microscopy (LSCM) creates thin optical
slices of living cells that are then used to monitor various mitochondrial
events in intact single cells throughout a period of time.
• Cytochrome c release from the mitochondria of living or fixed cells can
also be assayed using fluorescence and electron microscopy.
45.
46. Apoptosis in Cancer
• Apoptosis is regulated by two major genes p53 & Bcl-2
• Tumor suppressor p53 controls senescence and apoptosis in
response to damage.
• Mutations or overexpression of these genes will result in cancer.
• In moat cases, Bcl-2 expression has seen elevated
• Most cancer cells are defective in apoptotic response.
47.
48. Apoptosis in Neurodegenerative
Diseases
• Brain disorder that slowly destroys memory and thinking skills
• Apoptosis of hippocampal neurons in brain
1. Alzheimer's Disease:
2. Parkinson’s Disease:
• elevated activity of caspase-3 and increased expression of active caspase-3 in substantia
nigra.
• Apoptosis of the neurotransmitters Dopamine present in Substantia Nigra.
• Elevated levels of proapoptotic proteins, such as Bax, have also been seen in Parkinson’s
patients.
49. • rare, inherited disease that causes the progressive breakdown of nerve
cells in the brain.
• It usually effects person’s movement and thinking.
• In humans with HD, Caspases, among other proteins, cleave huntingtin
within the N-terminal region.
• Mutation in huntingtin may lead to apoptosis of neurons.
3. Huntington disease
50. Apoptosis & Necrosis
• Programmed Cell Death
• Induced by physiological stimuli
• No inflammation
• Shrinking of cytoplasm & condensation
of nucleus
• Blebbing of plasma membrane without
loss of integrity.
• ATP dependent pathways
Apoptosis Necrosis
• Premature cell death or tissue
• Induced by viruses, injury, infection
• Inflammation
• Swelling of cytoplasm and mitochondria
causing cell lysis.
• Loss of plasma membrane integrity
• No ATP is involved
51. • Programmed cell death which occurs in multicellular organisms.
• Characterized by specific morphological and biochemical features.
• Triggered by multi-signal pathways and regulated by extrinsic and
intrinsic ligands.
• Disordered apoptosis may lead to carcinogenesis and participates
in the pathogenesis of Alzheimer disease, Parkinson disease, AIDS
etc.
Conclusion