Apoptosis is a distinct type of cell death, in which the cell actively contributes to its own demise. The 'suicide program' is initiated by pathological changes in the cell's stimuli and in the environment. Apoptosis differs from necrosis in its morphological, biochemical and molecular biological characteristics. The series of events in apoptosis (apoptotic cascade) exhibits some differences depending on the cell type and stimuli. In general, the cytoplasmic level of ionized calcium elevates in an early phase, which activates calcium-dependent enzymes: endonucleases result in internucleosomal DNA-fragmentation and chromatin condensation, proteases disrupt the cytosceleton which leads to cell shrinkage, whereas transglutaminases crosslink cytoplasmic proteins with subsequent formation of cytoplasmic blebs and apoptotic bodies. The cell surface alterations induce cell phagocytosis without inflammation. In the regulation of this process several modulator genes, growth factors and receptors, cell-cycle regulators, ions, free radicals, enzymes and their interactions are involved. Apoptosis plays role in some of the neurological diseases, including cerebral ischemia. Apoptotic neurons are present as short as 10 minutes after the onset of focal cerebral ischemia, and are still detectable after 4 weeks. It has been suggested, that the apoptotic process can be initiated any time during the insult and for a relative long time thereafter. On the basis of this assumption, antiapoptotic treatment might effectively reduce cell loss and infarct size even days, or weeks after the ischemic insult. There are promising experimental results (e.g. introduction of anti-apoptotic genes and their protein products into the ischemic territory, receptor-mediated therapeutic strategies) to switch the cell's program from suicide to survival.
|Translated title of the contribution||The characteristics of apoptosis and its role in cerebral ischemia|
|Number of pages||10|
|Journal||Lege Artis Medicinae|
|Publication status||Published - Sep 26 1997|
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