Apoptosis is genetically programmed cell death that does not significantly affect neighboring cells and tissues. It is distinct from necrosis, which is an unregulated cell death destroying larger tissue areas.
Apoptosis is responsible for:
(i) death of intestinal mucosal cells as they reach the tip of the villus to be sloughed off;
(ii) death of epidermal cells as they reach the surface;
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(iii) death of large number of neurons in the CNS that do not make appropriate synaptic contact with their target organs; (iv) death of clones of lymphocytes that are likely to react with ‘self;
(v) removal of the webs between the fingers in fetal life;
(vi) regression of one or the other of Wollfian duct and Mullerian duct systems in the course of sexual differentiation in the fetus:
(vii) regression of incompletely developed Graafian follicles in ovary after ovulations;
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(viii) cyclic breakdown of the endometrium, leading to menstruation; (ix) lens protein ‘crystalline’ that is derived from the remnants of apoptotic cells.
The phases of apoptosis are induction, initiation, execution and disposal. The induction phase is the stage of gene activation. Several endogenous and exogenous stimuli activate the apoptotic genes through signal transduction.
In the initiation phase, the activated gene initiates a proteolytic cascade involving a family of proteases named caspases (cysteine aspartase). In the execution phase completes the death program.
The dying cell shrinks and loses its contact with neighboring cells. The cell DNA gets fragmented and the cytoplasm and chromatin condense. The nucleus and cytoplasm eventually fragment into multiple, small apoptotic bodies (karyorrhexis). The cytoplasmic blebs break away from the cell surface and eventually the entire cell breaks up (karyolysis). In the disposal phase, the cell remnants, called apoptotic bodies, are either phagocytosed, or are lost from the epithelial surfaces.