Cytoplasm apoptosis, programmed cell death

In some cells, dmg treatment and other stimuli can trigger a series of complex cytoplasmic biochemical reactions that appear to constitute a cellular suicide program, culminating in the degradation and compaction of chromatin. This programmed mode of cell death is known as apoptosis, and in nomral cellular conditions, it plays a considerable role in the early development of homeostasis of adult tissues. Apoptosis or literally programmed cell death, is so far known to be triggered by three major stimuli cell surface receptors such as FAS, mitochondrial response to stress, and cytotoxic T-cells. 

In addition to their critical role in protein synthesis, it has become clear that AARSs are involved in several other cellular pathways. Some AARSs regulate their own transcription and translation, while others contribute to splicing activities in mitochondria. Nuclear aminoacylation of tRNAs by imported AARSs is thought to be a quality control mechanism to ensure that only mature, fully active tRNAs are released efficiently to the cytoplasm for protein synthesis. Programmed cell death (apoptosis) also appears to have an AARS component—human tyrosyl-tRNA synthetase can be proteolytically cleaved into two polypeptides with distinct cytokine activities, despite the lack of such activity in the full-length TyrRS. It is likely that in time many more nontranslational functions of AARS will be identified. 

Apoptosis is characterized by nuclear chromatin condensation, cytoplasmic shrinking, a dilated endoplasmic reticulum, membrane blebbing, and the formation of apoptotic bodies. Programmed cell death is clean, quick, and involves a predictable sequence of structural changes that cause a cell to shrink and to be rapidly digested by macrophages or neighboring cells. 

Apoptosis is delayed and may be maximal at 24-48 h after an insult. However, apoptotic cells can be seen even within 6 h of an insult, but are not common. Apoptosis involves condensation of the nucleus. Condensation of the cytoplasm occurs with large vacuole formation. Some mitochondria may condense. Very uncommonly, some mitochondria swell in apoptosis. The cell splits up into membrane-bound apoptotic bodies that can be seen in the limit areas surrounding the core of an infarction. Apoptosis is a programmed form of cell death that occurs following a small but sufficient amount of damage to a cell. This initiates a program that eventually kills the cell. 

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