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 tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
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
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
1) Apoptosis is a process of programmed cell death that is important for normal development and physiology, as it helps remove excess, damaged, or dangerous cells.
2) It occurs through intrinsic and extrinsic pathways that involve caspase proteases and results in characteristic cell changes like blebbing and nuclear fragmentation.
3) Between 50-70 billion cells die per day in humans due to apoptosis, which is critical for processes like immune system maturation and tissue remodeling.
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.
The document summarizes programmed cell death or apoptosis. It describes apoptosis as a naturally occurring, genetically programmed process where a cell undergoes an organized breakdown. During apoptosis, cells shrink, break into membrane-bound fragments called apoptotic bodies, and are removed by phagocytes without causing inflammation. The document outlines the major pathways of apoptosis, including the intrinsic mitochondrial pathway and extrinsic death receptor pathway, and discusses the roles of caspase proteases and Bcl-2 family proteins in apoptosis signaling and regulation.
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.
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 tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
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
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
1) Apoptosis is a process of programmed cell death that is important for normal development and physiology, as it helps remove excess, damaged, or dangerous cells.
2) It occurs through intrinsic and extrinsic pathways that involve caspase proteases and results in characteristic cell changes like blebbing and nuclear fragmentation.
3) Between 50-70 billion cells die per day in humans due to apoptosis, which is critical for processes like immune system maturation and tissue remodeling.
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.
The document summarizes programmed cell death or apoptosis. It describes apoptosis as a naturally occurring, genetically programmed process where a cell undergoes an organized breakdown. During apoptosis, cells shrink, break into membrane-bound fragments called apoptotic bodies, and are removed by phagocytes without causing inflammation. The document outlines the major pathways of apoptosis, including the intrinsic mitochondrial pathway and extrinsic death receptor pathway, and discusses the roles of caspase proteases and Bcl-2 family proteins in apoptosis signaling and regulation.
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.
A detailed description of programmed cell death mechanism also called Apoptosis.
It explains about the factors, mechanism and pathways involved in the apoptosis.
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.
The document discusses cell cycle, cell death, necrosis, and apoptosis. It defines necrosis as unprogrammed cell death caused by external factors like trauma or toxins. Necrosis leads to cell membrane rupture and inflammation. The types of necrosis include coagulative, liquefactive, fat, caseous, and gangrenous necrosis. Apoptosis is defined as programmed cell death that occurs normally in development and to remove damaged cells. During apoptosis, cells shrink and fragment into apoptotic bodies without membrane rupture or inflammation. The mechanisms of apoptosis involve intrinsic and extrinsic pathways that activate caspase enzymes to break down cellular components in a regulated execution phase.
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.
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.
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.
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 is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
This document summarizes various mechanisms of cell death, including apoptosis and necrosis. Apoptosis, or programmed cell death, involves activation of caspases through intrinsic or extrinsic pathways, leading to controlled cell death without inflammation. Necrosis occurs due to external factors causing cell membrane rupture and inflammatory cell death. Other mechanisms discussed include autophagy, which involves lysosomal degradation of cellular components, and entosis, where one cell crawls inside another to die.
Cell death can occur through two main processes: apoptosis and necrosis. Apoptosis is programmed cell death that occurs under normal physiological conditions, triggered by intracellular signals. The cell shrinks and fragments into apoptotic bodies that are phagocytosed, avoiding inflammation. Necrosis is accidental cell death due to external factors like trauma or toxins, where the cell lyses and releases intracellular contents, potentially causing tissue damage and inflammation. Both processes are important for development, tissue homeostasis, and removal of damaged cells.
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
This document provides an introduction to apoptosis, or programmed cell death. It discusses how apoptosis is important for homeostasis and shaping tissues during development. Apoptosis is a highly regulated process where cells self-degrade through molecular machinery like caspases. The document outlines the molecular pathways of apoptosis, including the extrinsic, intrinsic, and execution pathways. It also discusses apoptosis in animals, plants, and the roles of autophagy and caspase enzymes.
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
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 also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
Seminar about apoptosis a type of programmed cell death in Soran University by Mahmood Khaleel Pirani (MSc Student) for Medical Physiology lecture on 24 November 2018
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
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.
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
There are two main forms of cell death: apoptosis and necrosis. Apoptosis is programmed cell death that occurs during normal cell turnover or in response to DNA damage. It involves nuclear fragmentation and formation of apoptotic bodies that are phagocytosed without inflammation. Necrosis is unregulated cell death due to injury and involves cell contents leaking out, triggering inflammation. There are several patterns of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis.
There is no inflammation in apoptosis because:
- Apoptosis is an orderly and controlled process of programmed cell death that does not release intracellular contents into the surrounding tissue.
- In apoptosis, the cell shrinks and its contents are packaged into apoptotic bodies which are then phagocytosed by neighboring cells or macrophages in a non-inflammatory manner.
- There is no disruption of the cell membrane or release of cytoplasmic enzymes and other inflammatory mediators that would trigger an inflammatory response, as occurs in necrosis. The orderly packaging and removal of dead cells prevents collateral tissue damage and inflammation.
A detailed description of programmed cell death mechanism also called Apoptosis.
It explains about the factors, mechanism and pathways involved in the apoptosis.
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.
The document discusses cell cycle, cell death, necrosis, and apoptosis. It defines necrosis as unprogrammed cell death caused by external factors like trauma or toxins. Necrosis leads to cell membrane rupture and inflammation. The types of necrosis include coagulative, liquefactive, fat, caseous, and gangrenous necrosis. Apoptosis is defined as programmed cell death that occurs normally in development and to remove damaged cells. During apoptosis, cells shrink and fragment into apoptotic bodies without membrane rupture or inflammation. The mechanisms of apoptosis involve intrinsic and extrinsic pathways that activate caspase enzymes to break down cellular components in a regulated execution phase.
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.
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.
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.
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 is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
This document summarizes various mechanisms of cell death, including apoptosis and necrosis. Apoptosis, or programmed cell death, involves activation of caspases through intrinsic or extrinsic pathways, leading to controlled cell death without inflammation. Necrosis occurs due to external factors causing cell membrane rupture and inflammatory cell death. Other mechanisms discussed include autophagy, which involves lysosomal degradation of cellular components, and entosis, where one cell crawls inside another to die.
Cell death can occur through two main processes: apoptosis and necrosis. Apoptosis is programmed cell death that occurs under normal physiological conditions, triggered by intracellular signals. The cell shrinks and fragments into apoptotic bodies that are phagocytosed, avoiding inflammation. Necrosis is accidental cell death due to external factors like trauma or toxins, where the cell lyses and releases intracellular contents, potentially causing tissue damage and inflammation. Both processes are important for development, tissue homeostasis, and removal of damaged cells.
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
This document provides an introduction to apoptosis, or programmed cell death. It discusses how apoptosis is important for homeostasis and shaping tissues during development. Apoptosis is a highly regulated process where cells self-degrade through molecular machinery like caspases. The document outlines the molecular pathways of apoptosis, including the extrinsic, intrinsic, and execution pathways. It also discusses apoptosis in animals, plants, and the roles of autophagy and caspase enzymes.
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
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 also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
Seminar about apoptosis a type of programmed cell death in Soran University by Mahmood Khaleel Pirani (MSc Student) for Medical Physiology lecture on 24 November 2018
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
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.
The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
There are two main forms of cell death: apoptosis and necrosis. Apoptosis is programmed cell death that occurs during normal cell turnover or in response to DNA damage. It involves nuclear fragmentation and formation of apoptotic bodies that are phagocytosed without inflammation. Necrosis is unregulated cell death due to injury and involves cell contents leaking out, triggering inflammation. There are several patterns of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis.
There is no inflammation in apoptosis because:
- Apoptosis is an orderly and controlled process of programmed cell death that does not release intracellular contents into the surrounding tissue.
- In apoptosis, the cell shrinks and its contents are packaged into apoptotic bodies which are then phagocytosed by neighboring cells or macrophages in a non-inflammatory manner.
- There is no disruption of the cell membrane or release of cytoplasmic enzymes and other inflammatory mediators that would trigger an inflammatory response, as occurs in necrosis. The orderly packaging and removal of dead cells prevents collateral tissue damage and inflammation.
The document discusses apoptosis, or programmed cell death. It defines apoptosis as a tightly regulated suicidal program in cells that activates enzymes to degrade the cell's own DNA and proteins. Apoptosis is important for normal development and tissue homeostasis by removing unwanted cells. The mechanisms of apoptosis involve both intrinsic pathways related to mitochondrial damage and extrinsic pathways activated by death receptors. Key regulators and effectors of apoptosis like caspases, Bcl-2 family proteins, and cytochrome c are discussed. Disorders related to too much or too little apoptosis can lead to conditions like neurodegeneration or cancer.
Difference between Apoptosis versus Necrosis and Types of Necrosis.pptxRukhshanda Ramzaan
Apoptosis Versus Nercosis
Apoptosis Necrosis
Predefined cell suicide or programmed cell death. Natural physiological Process. Involve one cell at a time. Cell shrinkage (Dense eosinophilic cytoplasm) Pyknosis (Condensation) and Karyorrhexis (fragmentation) of nuclear material Formation of membrane blebs and apoptotic bodies
Phagocytosis of apoptotic bodies by Macrophages
Caspase dependent pathway
No Inflammation (no immune response) Premature, unprogrammed cell death always pathological. Involve many cells Cell Swelling (Swelling of endoplasmic reticulum and mitochondria) and membrane blebs Pyknosis (condensation), Karyorrhexis (Fragmentation) and Karyolysis (lysis)of the nucleus. Breakdown of the plasma membrane, organelles (enzymatic digestion), leakage of cellular contents
Increased eosinophilia, Accumulation of Myelin figures (whorled precipitated Phospholipids)
Initiate Inflammation (Strong immune response)
This document provides an overview of necrosis and apoptosis. It defines necrosis as cell death resulting from external injury to cells, characterized by swelling and organelle breakdown. Apoptosis is defined as tightly regulated programmed cell suicide. The document discusses the morphology of necrosis under light microscopy and different types of necrosis. It then covers the mechanism, morphology, and triggers of apoptosis. Key differences between necrosis and apoptosis are that necrosis elicits inflammation while apoptosis does not and apoptosis is a tightly regulated process.
The document discusses various topics related to pathology including causes of cell injury, hypoxia, cellular adaptive responses, mechanisms of cell injury, features of reversible and irreversible injury, necrosis, apoptosis, calcification, pigmentation, and cellular aging. The key points are:
1. Hypoxia is the most common cause of cell injury, usually due to ischemia. Neurons are the most susceptible tissue to hypoxic damage.
2. Cellular adaptive responses to injury include atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.
3. Apoptosis is an active and programmed form of cell death, while necrosis is unprogrammed cell death due to severe injury
This document discusses various types of cellular adaptations, injuries, and deaths. It describes adaptations like hypertrophy and hyperplasia that occur in response to stress. It also discusses different types of cell injuries and deaths including necrosis, apoptosis, necroptosis, and pyroptosis. Various intracellular accumulations are also summarized such as lipids, proteins, glycogen, and pigments.
The document discusses various types of cell death including apoptosis, necrosis, autolysis, and gangrene. It provides details on the morphology, causes, and characteristics of each type. Apoptosis is defined as programmed cell death that is tightly regulated. It involves cell shrinkage, nuclear fragmentation, blebbing and formation of apoptotic bodies that are then phagocytosed. Necrosis is unregulated cell death caused by external factors like toxins and hypoxia. It results in cell swelling and lysosomal enzyme release. The document contrasts the features of apoptosis and necrosis and discusses the molecular pathways and caspase activation involved in apoptosis.
This document discusses apoptosis and necrosis. It begins by outlining the objectives of describing the differences between necrosis and apoptosis, the mechanisms and pathways of apoptosis, and implications of cellular aging. Necrosis is defined as progressive cell disintegration initiated by overwhelming stress, while apoptosis is a tightly regulated suicide program. The intrinsic mitochondrial pathway and extrinsic death receptor pathway converge in the execution phase through caspase activation, resulting in DNA fragmentation and phagocytosis of apoptotic bodies without inflammation. Physiologic and pathologic examples of apoptosis are provided.
Irreversible cellular injury can occur through two main types of cell death: necrosis and apoptosis. Necrosis is premature, unprogrammed cell death that is always pathological, occurring due to external factors like ischemia, toxins, or infections. It is characterized by loss of membrane integrity and inflammatory changes. Apoptosis is a normal, programmed form of cell death important for development, hormone regulation, and removing damaged cells. It occurs through an active enzymatic process and does not cause inflammation. Both pathways ultimately lead to cellular demise but differ significantly in their mechanisms and morphological appearance.
Necrosis is cell death resulting from progressive degenerative action of enzymes on lethally injured cells. It begins with impaired homeostasis leading to water and ion influx. Morphological changes include nuclear condensation or fragmentation, cytoplasmic eosinophilia, organelle damage, and membrane rupture. There are three main types - coagulative, liquefactive, and caseous. Coagulative necrosis occurs in solid organs from ischemia. Liquefactive necrosis results from enzymatic autolysis and hydrolysis. Caseous necrosis forms dry, cheesy material seen in tuberculosis. Necrosis causes inflammation while apoptosis is an orderly programmed cell death.
Apoptosis is a tightly regulated and genetically programmed form of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins. Cells undergoing apoptosis break into fragments called apoptotic bodies that are phagocytosed without eliciting inflammation. Apoptosis eliminates damaged or unneeded cells and plays an important role in development, tissue homeostasis, and the removal of infected or abnormal cells. It involves cell shrinkage, chromatin condensation, blebbing of the cell membrane, and the formation of apoptotic bodies that are phagocytosed without inflammatory response.
This document discusses apoptosis, or programmed cell death. It begins by defining apoptosis and describing its initial discovery. Key points made include: apoptosis is a genetically programmed process involving biochemical changes and morphological alterations; caspases play a central role by initiating and executing apoptosis; and inadequate or excessive apoptosis can contribute to diseases like cancer and neurodegenerative disorders. The document outlines the main biochemical changes in apoptosis and differences between apoptosis and necrosis. Disease associations with improper apoptosis levels are also reviewed.
Cell death occurs through two main forms: apoptosis and necrosis. Apoptosis is programmed cell death where cells undergo changes like DNA fragmentation and shrinkage in a way that avoids damaging nearby cells. Necrosis is unprogrammed cell death due to external factors like injury or internal issues. During necrosis, cells lose metabolic function and membrane integrity, organelles swell, and cell contents may leak out. Necrosis can occur through several types including coagulative, liquefactive, and gangrenous necrosis. Autophagy is a process where cells digest damaged organelles through the formation and fusion of vesicles to maintain cellular homeostasis.
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.
This document discusses cellular adaptation, injury, and death. It covers topics like hyperplasia, hypertrophy, atrophy, metaplasia, causes of cell injury including hypoxia and free radicals, necrosis and apoptosis. It provides detailed descriptions of the morphological changes that occur during cellular injury and the mechanisms of necrosis, apoptosis and intracellular accumulation.
This document discusses necrosis and apoptosis. It defines necrosis as the premature death of cells in living tissue due to irreversible injury. Necrosis can be caused by ischemia, physical agents, chemicals, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis. Treatment involves debridement and excision of dead tissue. Apoptosis is programmed cell death that occurs as part of normal development and tissue homeostasis. It is mediated by caspases and involves cell shrinkage, chromatin condensation, and fragmentation into apoptotic bodies that are phagocytosed. Dysregulation of apoptosis can contribute to diseases.
This document describes different types of cell injury and death, including reversible and irreversible injury. It discusses various causes of cell injury like hypoxia, toxins, and physical or chemical agents. The main types of cell death covered are necrosis and apoptosis. Necrosis is characterized by cell membrane disruption and inflammatory response, while apoptosis is a programmed, non-inflammatory form of cell death involving blebbing and formation of apoptotic bodies. The document contrasts the features of necrosis versus apoptosis and provides examples of different contexts in which each may occur.
This document provides an overview of cellular injury and cell death. It defines cell injury and explains the processes of reversible and irreversible injury. The mechanisms of cellular injury include impaired cell membrane function, decreased energy production, genetic alterations, and metabolic imbalances. Causes of injury include hypoxia, physical and chemical agents, infections, and free radicals. The document describes necrosis as irreversible cell injury involving enzymatic degradation and protein denaturation. Apoptosis is defined as a vital process of programmed cell death to eliminate unwanted cells. Morphological changes of necrosis and apoptosis are compared.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. Cellular adaption
• Atrophy- decrease in cell size
• Hypertrophy- increase in cell size
• Hyperplasia- increase in number of cells
• Metaplasia- one cell form to another
• Dysplasia- change is cellular shape
https://www.slideshare.net/DeepakKuma
rGupta2/cellular-adaptation-53513522
3.
4. Example of apoptosis in embryo
https://www.khanacademy.org/science/biology/developmental-biology/apoptosis-in-development/a/apoptosis
7. Apoptosis programmed cell death
• Apoptosis means- dropping off
• Reference to dropping off cell that are no
longer useful
• Part of normal development
– Apoptosis prunes the embryonic ducts during
gender specific development
• Tissue turnover
• Role in the immune system
• Undesirable cells
8. Role of apoptosis
Key roles in-
• Growth
• Immune surveillance
• Neoplastic development
https://slideplayer.com/slide/4446840/
12. Intrinsic apoptosis
• Bcl-2 controlled pathway
• Activation of caspases from inside the cell
• Formation of an intracellular caspase-9-activating
complex (apoptosome)
• Apoptosome forms after cytochrome c is released
from the mitochondria
14. Bcl-2 family
• Consists of a hydrophobic α-helix surrounded by amphipathic
α-helices
• Some members of the family have transmembrane domains at
their c-terminus
• Bcl2 stops channel formation on the surface of mitochondria so
cytochrome c not released through the channel
16. Caspase
• Cysteine protease
• The intrinsic apoptotic pathway is characterized by
permeabilisation of the mitochondria and release
of cytochrome c into the cytoplasm.
• Cytochrome c then forms a multi-protein complex
known as the "apoptosome" and initiates activation of
the caspase cascade through caspase 9
18. Overview of the apoptotic pathway
https://oncohemakey.com/the-scientific-basis-of-cancer/
19. Morphological features of apoptosis in
comparison
• Chromatin aggregation - nuclear and cytoplasmic
condensation to form apoptotic bodies
• Organelles remain intact
• Intact membrane surrounds apoptotic bodies
• No inflammatory response
• Apoptotic bodies phagocytosed by adjacent cells and
macrophages
• Typically affects isolated cells
• Surrounding cells remain in tact
22. Genetic defects in apoptosis
• Mutations rare but-
• Common mutation in Fas gene
• Mutation in FasL gene
• Caspase-1 mutation occurs rarely (NALP3
gene)
Autoimmune lymphoproliferative disorder
(ALPD)
23. Necrosis un-programmed cell
death
Necrosis means making dead
Accidental death of cells through-
• Injury
• Infection
• Cancer
• Infarction
• Toxins
• Inflammation
• No regulated signals to phagocytes to ‘clear’
necrotic cells and avoid immune surveillance
https://www.youtube.com/watch?v=vAYB6QWuOdM
25. Mechanism of necrosis
• Unable to pump out Na+
• Cell swells though osmosis
• Insult of necrosis injures many surrounding
cells
• Intracellular products initiate an inflammatory
response
• This can harm surrounding healthy tissues
26. Detailed events of necrosis
• Cell shrinkage and rounding occur because of the
retraction lamellipodia and the breakdown of the proteinaceous
cytoskeleton by caspases.
• Mitochondria become ‘leaky’
• The cytoplasm appears dense, and the organelles appear tightly
packed.
• Chromatin undergoes condensation into compact patches against
the nuclear envelope (also known as the perinuclear envelope) in a
process known as pyknosis, a hallmark of apoptosis.
• The nuclear envelope becomes discontinuous and the DNA inside it
is fragmented in a process referred to as karyorrhexis. The nucleus
breaks into several discrete chromatin bodies ornucleosomal
units due to the degradation of DNA
27. Cell shrinkage and rounding occur because of the
retraction lamellipodia and the breakdown of the proteinaceous
cytoskeleton by caspases.
31. Morphological features of Necrosis
Cell membrane integrity lost and lysosomal hydrolases
released, resulting in -
• Nuclei small, condensed
• Pyknosis- nuclei stain deeply with hematoxylin (basophilic)
• Karyorrhexis- nuclei fragmented into particles
• Karyolysis- nuclear lysis
• Cytoplasm deeply eosinophilic (RNA loss, protein
coagulation)
• Typically affects large groups of cells
33. Morphological patterns of Necrosis
• Coagulative necrosis, typically in hypoxic cells with few
lysosomes
• MI
• Infarct of spleen
• Liquifactive necrosis in cells with numerous lysosomes
or where bacteria attract neutrophils
• Pneumonia
• Brain hypoxia
• Gummatous necrosis restricted to spirochaetal infections
• Syphylis
• Haemorrhagic necrosis - blockage of venous drainage
of tissue or organ
• eg. Testicular torsion
34. Types of necrosis
Coagulative necrosis Liquefactive necrosis
Digestive release of lysosomal enzymes
turn tissue into pus (CNS)
Can also occur in lungs with abscesses
Typically occurs with infarcts or ischemia
Architecture of dead tissue preserved
`regeneration can occur with enough viable cells
35. Types of necrosis
Fat necrosis Fibrinoid necrosis
Seen in autoimmune diseases, vasculitisChalky white deposites
36. Examples of different types of necrosis
Caseous necrosis
Cheese like, yellow-white area
Combines features of Coagulative and liquefative.
Found in centre of tuberculous infections
Gumatous necrosis
Rubbery texture of tissue of the hard pallet
37. Diseases associated with necrosis
• Autoimmune vasculitis
• Peripheral vascular disease
• Osteonecrosis of the jaw
• Aseptic bone necrosis
• Gangrene
• Ishaemic cascade (stroke)
• Necrotoxins cause necrosis
• Cystic medial necrosis
• Tumour necrosis due to hypoxia-angiogenesis
Gangrenous necrosis
38. Irreversible versus reversible necrosis
Irreversible
• Cell digestion by lytic
enzymes
• Protein denaturation
• Hypoxia, chemical and
physical agents, microbial,
immunological injury
Reversible
43. Cell Death
Necrosis
• Pathological cell death - external factors
• Hypoxia, chemical toxins cause necrosis
• Damage to cell physiology
• Degradation of the cell
• Influx of water and ions
• Cellular organelles swell and rupture
Apoptosis
• Programmed or physiological cell death
• Constituent genes cause cell death
46. Morphological patterns of Necrosis
• Coagulative necrosis, typically in hypoxic cells with few
lysosomes
• MI
• Infarct of spleen
• Liquifactive necrosis in cells with numerous lysosomes
or where bacteria attract neutrophils
• Pneumonia
• Brain hypoxia
• Gummatous necrosis restricted to spirochaetal infections
• Syphylis
• Haemorrhagic necrosis - blockage of venous drainage
of tissue or organ
• eg. Testicular torsion
47. Diseases associated with necrosis
• Autoimmune vasculitis
• Peripheral vascular disease
• Osteonecrosis of the jaw
• Aseptic bone necrosis
• Gangrene
• Ishaemic cascade (stroke)
• Necrotoxins cause necrosis
• Cystic medial necrosis
• Tumour necrosis due to hypoxia-angiogenesis
48. Etiological Importance of Apoptosis
• Suppressed apoptosis
– Neoplasia
– Autoimmunity
• Abnormally induced
– AIDS
– Neurodegenerative disease