Apoptosis
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Apoptosis is a genetically programmed cell death process that eliminates unwanted cells through activation of caspases. There are two main pathways that activate caspases - the extrinsic death receptor pathway where ligands bind to cell surface receptors, and the intrinsic mitochondrial pathway where increased permeability of mitochondria releases proteins that activate caspase. The Bcl-2 family of proteins regulate apoptosis by integrating both pro-apoptotic and anti-apoptotic signals to determine if a cell should undergo programmed cell death.
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Cell death
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.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Apoptosis
The document discusses apoptosis, or programmed cell death. It defines apoptosis and describes the morphological changes that occur during apoptosis, including cell shrinkage, nuclear fragmentation, and chromatin condensation. It then explains the role of caspases in apoptosis, the intrinsic and extrinsic pathways that initiate apoptosis, and the common pathway involving caspase activation that leads to apoptosis. The document concludes by discussing disorders related to improper apoptosis and references several sources for further information.
Apoptosis
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.
Cell injury. intracellular extracellular accumulation
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
Apoptosis
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
Mechanisms of cell injury
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
Cell injury : Intracellular accumulations
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
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Cell death
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.
Apoptosis
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Apoptosis
The document discusses apoptosis, or programmed cell death. It defines apoptosis and describes the morphological changes that occur during apoptosis, including cell shrinkage, nuclear fragmentation, and chromatin condensation. It then explains the role of caspases in apoptosis, the intrinsic and extrinsic pathways that initiate apoptosis, and the common pathway involving caspase activation that leads to apoptosis. The document concludes by discussing disorders related to improper apoptosis and references several sources for further information.
Apoptosis
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.
Cell injury. intracellular extracellular accumulation
Cell injury and alterations can occur through various causes and result in reversible or irreversible changes to cells. Reversible cell injury may allow the cell to return to normal, while irreversible injury leads to cell death through necrosis or apoptosis. Specific patterns of acute cell injury include cellular swelling and fatty change. Long-term or persistent stimuli can also result in subcellular alterations and intracellular accumulations of substances such as lipids, proteins, pigments, and more. Extracellular accumulations may involve changes to collagen, elastic fibers, proteoglycans, and basement membranes in connective tissue.
Apoptosis
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
Mechanisms of cell injury
Cellular injury occurs when stress exceeds a cell's ability to adapt and can be caused by factors like oxygen deprivation, toxins, infections, or genetic mutations. The main mechanisms of cellular injury include ATP depletion, mitochondrial damage, loss of calcium homeostasis, accumulation of reactive oxygen species, defects in membrane permeability, and damage to DNA and proteins. Without adequate response to injury, irreversible damage occurs through mechanisms like lipid peroxidation, DNA fragmentation, and protein cross-linking, ultimately leading to cell necrosis.
Cell injury : Intracellular accumulations
Intracellular accumulations can occur through the buildup of various cellular constituents, including fat, proteins, carbohydrates, and pigments. Fatty change is the accumulation of triglycerides in cells, commonly seen in liver cells due to alcohol abuse, obesity, or other metabolic derangements. Proteins can accumulate intracellularly in conditions like myeloma or nephrotic syndrome. Glycogen storage diseases result in glycogen accumulation in cells. Pigment accumulations include lipofuscin, melanin, hemosiderin, and exogenous pigments like carbon. These accumulations can be transient or permanent and range from harmless to toxic.
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 injury 2
1. The document describes the morphological changes that occur in cells undergoing reversible injury, irreversible injury, necrosis, and apoptosis as observed by light and electron microscopy.
2. Key differences are noted between necrosis, which involves the uncontrolled digestion of cells and release of cellular contents, versus apoptosis, which is a tightly regulated form of programmed cell death where cells break into fragments that are phagocytosed without inflammation.
3. Examples are provided of physiological apoptosis during development and tissue remodeling, as well as pathological apoptosis resulting from DNA damage, misfolded proteins, viral infections, and organ atrophy.
Spread of tumours
Tumors can spread through direct extension into surrounding tissues, through the lymphatic or vascular systems, or by transcoelomic spread through body cavities. Lymphatic spread is common for carcinomas and follows drainage routes to regional lymph nodes. Vascular spread occurs via blood vessels either as tumor emboli or growing along vessel walls. Certain primary tumors have tendencies to metastasize to specific organs, such as prostate cancer spreading to bone. Transcoelomic spread involves cavities such as the peritoneal, pleural, or pericardial spaces, potentially causing malignant ascites or pleural effusions. Perineural spread grows along nerve bundles.
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Reversible cell injury occurs when cells are exposed to a brief period of ischemia or hypoxia. This causes 1) decreased ATP generation, 2) intracellular lactic acidosis and nuclear clumping, 3) damage to plasma membrane pumps causing sodium accumulation and calcium influx, and 4) reduced protein synthesis. If the stressor is removed quickly, the cell injury may be reversible and the cell can return to normal functioning.
Irreversible cell injury
The molecular mechanisms connecting cell injury to cell death are complex and not fully understood. There are many potential causes of cell injury that may or may not be fatal, and the "point of no return" where damage becomes irreversible is still unclear. Additionally, cells can die through different pathways, making the definition of irreversible injury difficult. Cell injury can result in either reversible or irreversible cell death through mechanisms like apoptosis, the body's normal programmed cell death process, or necrosis, pathological cell death resulting in inflammation.
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.
Cellular ageing
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This document discusses cell injury, adaptations, and degenerations in pathology. It begins by defining key terms like etiology, pathogenesis, and morphology. It then explains the causes of cell injury including hypoxia, physical agents, chemicals, microbes, and immune reactions. The document delves into the pathogenesis of cell injury, noting factors like the type, duration, and severity of the injurious agent and target cell characteristics. It also describes the mechanisms of cell injury such as ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects. Finally, it distinguishes between reversible and irreversible cell injury.
Free radical induced injury
Free radicals are highly unstable chemical species with unpaired electrons that can damage cells. Reactive oxygen and nitrogen species are important free radicals generated through normal cellular processes and environmental exposures that can initiate chain reactions. Free radicals attack and degrade membranes, proteins, and nucleic acids. This can lead to lipid peroxidation, protein oxidation, and DNA damage implicated in various diseases. Cells employ antioxidant defenses and enzymes like catalase and superoxide dismutase to limit free radical damage.
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PROGRAMMED CELL DEATH (APOPTOSIS )
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.
Pathology cell injury i
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Cellular ageing
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
Inflammatory mediators
This document summarizes different mediators of inflammation. It describes cell-derived mediators like vasoactive amines (histamine, serotonin), arachidonic acid metabolites from cyclooxygenase and lipoxygenase pathways, lysosomal components, platelet activating factor, cytokines, and nitric oxide. It also discusses plasma-derived mediators including the kinin system, clotting system, fibrinolytic system, and complement system. These mediators cause effects like vasodilation, increased vascular permeability, adhesion of leukocytes, and chemotaxis during inflammation.
Apoptosis
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.
healing and tissue repair
Tissue repair occurs through either regeneration or scar formation. Regeneration involves the proliferation of residual cells to completely restore lost tissue, while scar formation deposits connective tissue when regeneration is not possible. The key stages of wound healing are inflammation, proliferation, granulation tissue formation, wound contraction, and strength acquisition. Factors like nutrition, infection, and location can influence healing. Complications include deficient or excessive scarring, contractures, and exuberant granulation. Stem cells also contribute to tissue repair through self-renewal and generation of new cells.
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
Apoptosis
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 by dr Alfarah.pptx
1) Apoptosis is a tightly regulated form of programmed cell death that occurs as a normal physiological process or in pathological conditions. It is characterized by cell shrinkage, chromatin condensation, DNA fragmentation, and formation of membrane-bound apoptotic bodies that are phagocytosed without inflammation.
2) The intrinsic and extrinsic pathways regulate apoptosis through a cascade of caspase activation. The intrinsic pathway involves mitochondrial permeabilization and cytochrome c release in response to cellular stress. This activates caspase-9 and downstream executioner caspases like caspase-3. The extrinsic pathway is triggered via death receptors engaging caspase-8 and -10. Both pathways converge on caspase activation and cell dismantling.
3)
Apoptosis
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
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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 injury 2
1. The document describes the morphological changes that occur in cells undergoing reversible injury, irreversible injury, necrosis, and apoptosis as observed by light and electron microscopy.
2. Key differences are noted between necrosis, which involves the uncontrolled digestion of cells and release of cellular contents, versus apoptosis, which is a tightly regulated form of programmed cell death where cells break into fragments that are phagocytosed without inflammation.
3. Examples are provided of physiological apoptosis during development and tissue remodeling, as well as pathological apoptosis resulting from DNA damage, misfolded proteins, viral infections, and organ atrophy.
Spread of tumours
Tumors can spread through direct extension into surrounding tissues, through the lymphatic or vascular systems, or by transcoelomic spread through body cavities. Lymphatic spread is common for carcinomas and follows drainage routes to regional lymph nodes. Vascular spread occurs via blood vessels either as tumor emboli or growing along vessel walls. Certain primary tumors have tendencies to metastasize to specific organs, such as prostate cancer spreading to bone. Transcoelomic spread involves cavities such as the peritoneal, pleural, or pericardial spaces, potentially causing malignant ascites or pleural effusions. Perineural spread grows along nerve bundles.
Reversible cell injury I Pathology
Reversible cell injury occurs when cells are exposed to a brief period of ischemia or hypoxia. This causes 1) decreased ATP generation, 2) intracellular lactic acidosis and nuclear clumping, 3) damage to plasma membrane pumps causing sodium accumulation and calcium influx, and 4) reduced protein synthesis. If the stressor is removed quickly, the cell injury may be reversible and the cell can return to normal functioning.
Irreversible cell injury
The molecular mechanisms connecting cell injury to cell death are complex and not fully understood. There are many potential causes of cell injury that may or may not be fatal, and the "point of no return" where damage becomes irreversible is still unclear. Additionally, cells can die through different pathways, making the definition of irreversible injury difficult. Cell injury can result in either reversible or irreversible cell death through mechanisms like apoptosis, the body's normal programmed cell death process, or necrosis, pathological cell death resulting in inflammation.
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.
Cellular ageing
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
Cell injury and degenerations
This document discusses cell injury, adaptations, and degenerations in pathology. It begins by defining key terms like etiology, pathogenesis, and morphology. It then explains the causes of cell injury including hypoxia, physical agents, chemicals, microbes, and immune reactions. The document delves into the pathogenesis of cell injury, noting factors like the type, duration, and severity of the injurious agent and target cell characteristics. It also describes the mechanisms of cell injury such as ATP depletion, mitochondrial damage, calcium influx, oxidative stress, and membrane permeability defects. Finally, it distinguishes between reversible and irreversible cell injury.
Free radical induced injury
Free radicals are highly unstable chemical species with unpaired electrons that can damage cells. Reactive oxygen and nitrogen species are important free radicals generated through normal cellular processes and environmental exposures that can initiate chain reactions. Free radicals attack and degrade membranes, proteins, and nucleic acids. This can lead to lipid peroxidation, protein oxidation, and DNA damage implicated in various diseases. Cells employ antioxidant defenses and enzymes like catalase and superoxide dismutase to limit free radical damage.
Neoplasia Characteristics and classification of cancer
This document provides an overview of neoplasia and tumor characteristics and classification. It defines neoplasia as new abnormal cell growth that can be benign or malignant. Benign tumors remain localized, while malignant tumors invade surrounding tissues and metastasize to distant sites. Tumors are classified based on tissue of origin, degree of differentiation, growth patterns, and whether they are benign or malignant. Malignant tumors are generally less differentiated, grow and spread more rapidly, and invade locally and metastasize, making them more difficult to treat. The document also discusses cellular adaptations, causes of cancer, tumor properties, grading, staging, and nomenclature used in tumor classification.
Extra Cellular Matrix (ECM)
The document discusses the extracellular matrix (ECM), which provides structural and biochemical support to surrounding cells. It is composed of proteins, enzymes and glycoproteins such as collagen, fibronectin and laminin. The ECM regulates cell communication, stores growth factors, and influences cell behavior through mechanical properties. Defects in ECM proteins can cause connective tissue disorders like Marfan syndrome, osteogenesis imperfecta and Ehlers-Danlos syndrome. The ECM is important for tissue development, wound healing and has applications in medicine.
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describes all the theories , hallmarks and various cancer related genetic factors with an emphasis on oral cancer
PROGRAMMED CELL DEATH (APOPTOSIS )
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.
Pathology cell injury i
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
Cellular ageing
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
Inflammatory mediators
This document summarizes different mediators of inflammation. It describes cell-derived mediators like vasoactive amines (histamine, serotonin), arachidonic acid metabolites from cyclooxygenase and lipoxygenase pathways, lysosomal components, platelet activating factor, cytokines, and nitric oxide. It also discusses plasma-derived mediators including the kinin system, clotting system, fibrinolytic system, and complement system. These mediators cause effects like vasodilation, increased vascular permeability, adhesion of leukocytes, and chemotaxis during inflammation.
Apoptosis
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.
healing and tissue repair
Tissue repair occurs through either regeneration or scar formation. Regeneration involves the proliferation of residual cells to completely restore lost tissue, while scar formation deposits connective tissue when regeneration is not possible. The key stages of wound healing are inflammation, proliferation, granulation tissue formation, wound contraction, and strength acquisition. Factors like nutrition, infection, and location can influence healing. Complications include deficient or excessive scarring, contractures, and exuberant granulation. Stem cells also contribute to tissue repair through self-renewal and generation of new cells.
Cell injury: causes, pathogenesis, Morphology of reversible cell injury
The document discusses cell injury and its mechanisms. It describes how cells can become injured through various stressors like hypoxia, physical/chemical agents, infections, etc. This causes damage to key cellular components like membranes, respiration, and DNA. The injury can be reversible through mild changes like hydropic swelling, or progress to irreversible necrosis or apoptosis if the cell cannot adapt. Free radicals are also discussed as a mediator of injury through lipid peroxidation, protein/DNA oxidation, and cytoskeletal damage. Examples of reversible changes include hydropic swelling seen as cloudy vacuoles, while irreversible injury leads to cell death.
Apoptosis
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
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Similar to Apoptosis
APOPTOSIS by dr Alfarah.pptx
1) Apoptosis is a tightly regulated form of programmed cell death that occurs as a normal physiological process or in pathological conditions. It is characterized by cell shrinkage, chromatin condensation, DNA fragmentation, and formation of membrane-bound apoptotic bodies that are phagocytosed without inflammation.
2) The intrinsic and extrinsic pathways regulate apoptosis through a cascade of caspase activation. The intrinsic pathway involves mitochondrial permeabilization and cytochrome c release in response to cellular stress. This activates caspase-9 and downstream executioner caspases like caspase-3. The extrinsic pathway is triggered via death receptors engaging caspase-8 and -10. Both pathways converge on caspase activation and cell dismantling.
3)
Apoptosis
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 for first semester
Apoptosis is a form of programmed cell death that is vital for normal development and tissue homeostasis. It occurs through two main signaling pathways - the extrinsic pathway activated by death receptors, and the intrinsic pathway involving the mitochondria. The intrinsic pathway is regulated by Bcl-2 proteins and relies on the release of cytochrome c from mitochondria to activate caspases through a proteolytic cascade, leading to characteristic biochemical changes including DNA fragmentation. Disturbances in apoptosis can contribute to degenerative disorders, autoimmunity, and cancer.
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 seminar
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 regulation by BCL-2
This document summarizes apoptosis regulation by Bcl-2 family proteins. It describes how Bcl-2 family proteins like Bcl-2 and Bax regulate apoptosis by controlling mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. Cytochrome c then activates caspase-9, leading to a caspase cascade that executes apoptosis. The Bcl-2 family contains both pro-apoptotic and anti-apoptotic members that regulate this process by interacting with each other to control mitochondrial membrane integrity and the apoptotic program.
physiology of apoptosis first year mbbs medical.pdf
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.
Apoptosis in health and diseases
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.pdf
Apoptosis is a tightly regulated form of programmed cell death that involves the activation of caspases. There are intrinsic and extrinsic pathways of apoptosis. The intrinsic pathway involves signals within the cell such as DNA damage, causing mitochondrial membrane permeabilization and cytochrome c release. This forms the apoptosome and activates caspase-9 and caspase-3. The extrinsic pathway involves death receptors and activates caspase-8. Caspases cleave cellular proteins leading to cell death. Phagocytes then engulf and degrade the apoptotic bodies. Other forms of regulated cell death include necroptosis, pyroptosis and ferroptosis.
Apoptosis
Apoptosis, or programmed cell death, is an important process by which cells self-destruct in a regulated manner. During development, apoptosis sculpted structures like fingers and toes by killing cells between them. Apoptosis also causes tissues like the tail to disappear at metamorphosis. The process is mediated by caspase proteases and regulated by Bcl-2 family proteins, with Bax and Bak activating caspases. Cells undergo apoptosis to maintain tissue homeostasis, avoid harming neighbors, and be removed by macrophages.
Intrinsic and Extrinsic Pathway of Apoptosis
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.
Cell Death and Cancer
Cell death, or apoptosis, is a tightly regulated process that is essential for development and tissue homeostasis. It occurs through two main pathways: the death receptor pathway and the mitochondrial pathway. The balance between pro-apoptotic and anti-apoptotic BCL-2 family proteins determines whether a cell undergoes apoptosis. Caspases are cysteine proteases that are either initiators or executioners of apoptosis. Impaired apoptosis can lead to diseases like cancer, autoimmunity, and neurodegeneration. Necrosis was traditionally thought to be unregulated cell death, but recent evidence shows some forms of necrosis can be programmed.
Apoptosis
Apoptosis is a programmed cell death process where cells activate enzymes to degrade their own DNA and proteins. It is essential for development, homeostasis, and defense against cancer. The molecular mechanisms of apoptosis involve caspase-dependent pathways - the extrinsic pathway triggered by death receptors and the intrinsic pathway initiated within mitochondria by stress signals. These pathways activate initiator caspases that then activate executioner caspases to degrade cellular proteins and induce apoptosis. Tight regulation of apoptosis is important as its dysfunction can lead to degenerative diseases or cancer.
Cell death,regulators, apoptosis,necrosis,autophagy
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.
Apoptosis
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
6. apoptosis mdzah- sp sinhasan
Apoptosis is a tightly regulated form of programmed cell death that occurs through activation of intracellular enzymes. It plays an important role in physiological processes like embryogenesis and pathological conditions like viral infections. During apoptosis, cells shrink and their chromatin condenses. This leads to formation of apoptotic bodies that are phagocytosed by macrophages. The process is controlled through signaling pathways and mitochondrial permeability, which activate caspase enzymes that degrade DNA and proteins, cross-link proteins, and mark the cell for phagocytosis. Understanding apoptosis provides insights into development, disease mechanisms, and potential therapies.
apopwqgdcbhuredgbcfyhhvhcctosis (1).pptx
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
Apoptosis is a programmed cell death process that occurs normally during development and aging and as a defense mechanism. There are two main pathways of apoptosis - the intrinsic mitochondrial pathway initiated from within the cell, and the extrinsic death receptor pathway initiated from outside the cell. Both pathways involve caspase proteins that activate a caspase cascade leading to characteristic cell changes and death. Apoptosis must be tightly regulated as both insufficient and excessive apoptosis can lead to disorders.
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.
power point presentatio in biochemistry 2024
The document discusses how cancer cells evade apoptosis or programmed cell death. It describes the two main pathways of apoptosis - intrinsic and extrinsic - and how they activate caspase proteases to kill cells. Cancer cells resist apoptosis through several mechanisms: 1) Overexpressing anti-apoptotic proteins like Bcl-2, 2) Suppressing or destroying pro-apoptotic proteins, 3) Altering protein functions through phosphorylation, and 4) Modulating gene and protein expression transcriptionally or translationally. The most common way is disabling the p53 tumor suppressor gene in over half of cancers.
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Cell death,regulators, apoptosis,necrosis,autophagy
Cell death,regulators, apoptosis,necrosis,autophagy
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Sarcoma
Sarcoma represents 1% of all malignant tumors and includes soft tissue sarcomas (STS), bone sarcomas, and visceral sarcomas. STS are more common than bone sarcomas by a ratio of 4:1. Risk factors for sarcoma include genetic syndromes, radiation exposure, and certain chemical exposures. Diagnosis involves imaging such as MRI or CT along with pathological confirmation. Treatment depends on the location and stage of disease, and may involve surgery, radiation therapy, chemotherapy, or targeted therapy. The goal is curative treatment for localized disease and palliation for metastatic disease.
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H & N cancer
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Testicular cancer
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Cancer genes can be divided into two main classes: oncogenes and tumor suppressor genes. Oncogenes promote cell growth and proliferation when activated by mutations, while tumor suppressor genes normally inhibit cell growth and their inactivation allows for unchecked cell division. Dysfunction of multiple cancer genes is typically required for malignant transformation, as an imbalance between oncogene and tumor suppressor gene activity leads to cancer development. Common oncogenes include ras, myc, and HER2, while tumor suppressor genes include RB, p53, and APC. Mutations in DNA repair genes can also contribute to cancer by allowing genetic errors to persist.
Cell cycle
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Cancer metastasis
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2) Key steps include degradation of the extracellular matrix, entry and survival in the circulation, arrest and extravasation at distant sites, and induction of angiogenesis to establish blood supply for growing tumors.
3) Factors such as matrix metalloproteinases, integrins, and angiogenic growth factors regulate these steps by promoting degradation of barriers, cell adhesion, and new blood vessel formation to enable metastatic tumors to grow.
Hallmarks of cancer
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Carcinogenesis
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2) The multihit hypothesis proposes cancer develops through accumulation of multiple genetic mutations in oncogenes and tumor suppressor genes, requiring 4-5 mutations for malignancy.
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Neoplasia
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Apoptosis
- 1. Apoptosis Mohammed Fathy Bayomy, MSc, MD Lecturer Clinical Oncology & Nuclear Medicine Faculty of Medicine Zagazig University
- 2. Apoptosis Definition: Apoptosis is defined as a distinctive active, genetically programmed cell death which eliminates unwanted cells. Literally, apoptosis in Greek language means falling of leaves of trees in winter Character * May be physiological or pathological * Resulting from mild injuries * Affects single isolated cells * Nonviable cell constituents shrink & are enclosed by cell membranes, absence of inflammatory reaction
- 4. Pathogenesis: enzymes are activated by calcium ions, cytochrome-C, Apaf-1 & ceramide * Enzymatic cleavage of cytoskeleton protein by cysteine proteases (caspases) * Protein cross-linking by transglutaminases * Cleavage of DNA by several agents, including enzymes endonuclease Pathways: two enzymes activation pathways 1) Extrinsic (Death receptor) pathway FAS ligand (soluble or membrane-bound) will bind to FAS cell membrane receptor or cytokine tumor necrosis factor (TNF) will bind to its receptor (TNFR) on cell membrane activation of membrane-bound protein FADD caspase activation
- 5. 2) Intrinsic (Mitochondrial integrity) pathway Increase of mitochondrial permeability release of calcium & cytochrome-C from mitochondria to cytosol assembly of apoptotic protease activating factor (Apaf-1) activates caspases
- 6. Genetic control of Apoptosis Bcl-2 family members are decision-makers that integrate pro-apoptotic and anti-apoptotic signals to determine whether cell should commit suicide 1) Anti-apoptotic Bcl-2 type proteins * Including Bcl-2, Bcl-xL, Bcl-wL * Two ways of antagonizing death signals - They insert into outer mitochondrial membrane to antagonize channel-forming pro-apoptotic factors cytochrome c release - Bind cytoplasmic Apaf so that it cannot form apoptosome complex
- 7. 2) Pro-apoptotic Bcl-2 type proteins * Pro-apoptotic ion channel forming members (Bax, Bak, Bok, Bcl-xs) when they dimerize with pro-apoptotic BH3-only members in outer mitochondrial membrane, they form an ion channel that promotes cytochrome c release rather than inhibiting it * Pro-apoptotic BH3-only proteins (Bad, Bid, Bom/Bim) activates pro-apoptotic family members (Bax) & inactivates anti-apoptotic members (Bcl-2)