Apoptosis is otherwise called programmed cell death. It is an essential process for multicellular organism growth and development. It is a highly-organized process.
During apoptosis classical apoptotic cell death, heterochromatin forms from chromatin and moves towards the nuclear periphery of the cell.The Cell contents of an apoptotic cell remain membrane-bound as apoptotic bodies, which are then phagocytized, causing no disruption such as inflammation.Apototic necrotic cells typically expell their contents into the extracellular space, eliciting an inflammatory response .
Steps in apoptosis.
The major steps are:
Shrinking and rounding of the cell membrane.
DNA distruction or fragmentationt hrough chromatin condensation and DNA compaction.
Condensation of cytoplasm and cell organelles.
Vesicle formation by membrane blebbing and formation of apoptotic bodies.
Phagocytosis of the apoptotic BODIES.
Intrinsic pathway of apoptosis:
AmApoptotic protease activating factor 1, Procapases 2, 3,aVnd 9, latent AlF, and cytochrome C exist in the mitochondriali ntermembrane space.
Upon release of these apoptosis-inducing factors into the cytplasm the cytochrome C forces the cleavage of caspase 9.
Caspase 9 is the initiator caspace, which then activatesc aspases 3, 6, and 7. Effector caspases are activated and thesee ventually cause cell death.
Extrinsic pathway of apoptisis:
The extrinsic pathway of apoptosis is activatedb inding of a death ligand to a death receptor on the cell membrane . Death receptors are FAS and TNF receptors anda ctivated by FAS or TNF ligands. Activation of these receptorscauses the cleavage of initiator caspases within thec ytoplasm. This then activates downstream effector caspases,ultimately leading to cell death.
During apoptosis classical apoptotic cell death, heterochromatin forms from chromatin and moves towards the nuclear periphery of the cell.The Cell contents of an apoptotic cell remain membrane-bound as apoptotic bodies, which are then phagocytized, causing no disruption such as inflammation.Apototic necrotic cells typically expell their contents into the extracellular space, eliciting an inflammatory response .
Steps in apoptosis.
The major steps are:
Shrinking and rounding of the cell membrane.
DNA distruction or fragmentationt hrough chromatin condensation and DNA compaction.
Condensation of cytoplasm and cell organelles.
Vesicle formation by membrane blebbing and formation of apoptotic bodies.
Phagocytosis of the apoptotic BODIES.
Intrinsic pathway of apoptosis:
AmApoptotic protease activating factor 1, Procapases 2, 3,aVnd 9, latent AlF, and cytochrome C exist in the mitochondriali ntermembrane space.
Upon release of these apoptosis-inducing factors into the cytplasm the cytochrome C forces the cleavage of caspase 9.
Caspase 9 is the initiator caspace, which then activatesc aspases 3, 6, and 7. Effector caspases are activated and thesee ventually cause cell death.
Extrinsic pathway of apoptisis:
The extrinsic pathway of apoptosis is activatedb inding of a death ligand to a death receptor on the cell membrane . Death receptors are FAS and TNF receptors anda ctivated by FAS or TNF ligands. Activation of these receptorscauses the cleavage of initiator caspases within thec ytoplasm. This then activates downstream effector caspases,ultimately leading to cell death.
Significance
1. Apoptosis is important in every day of our lives, as many processes depends
on apoptosis to occur. Furthermore, research has shown that the inhibition
or hyperactivity of apoptosis can cause disease.
2. Apoptosis is vital for the formation of digits, organs and Ilimbs in
embryogenesis
3. Apoptosis is needed in the strict process of tissue homeostasis in the
developed animal
4. Increased apoptosis causes the vascular calcification seen in end-stage
kidney failure.
5. Increased apoptosis can Ilead to larger plaque formation in coronary heart
disease
6. Decreased apoptosis is seen in many aggressive cancers, chemotherapy
targets cancer cells and induces them to die
7.In arthrtitis, the increased levels of inflammation cause continual activation of cell death leading to the degradation and damage of affected joints
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