engleski

Telomeres as main mechanism of aging

Most normal mammalian cell lines demonstrate a common growth pattern during proliferation in vitro. Young cultures initially have a period of rapid growth during which the majority of the cells divide vigorously. As the culture accumulates more divisions the growth potential declines due to the gradual increase in the fraction of nondividing, senescent cells. Eventually, the entire culture enters the terminally nondividing state referred to as replicative senescence (1, 2). Upon growth cessation, senescent cells do not die but remain viable in culture, undergoing various morphological and biochemical changes, e. g. cell size enlargement, lack of 3H-thymidine incorporation, endogenous senescence associated (SA)--gal staining at pH6 (2, 3, 4) as well as altered gene expression (5). However, the introduction of various viral proteins that impair p53 and pRB functions results in an extended lifespan followed by entry into crisis and occasionally the emergence of immortal clones. It has been proposed that these and other phenomena have their origins in processes related to the maintenance of telomeres, which are repetitive sequences at the end of all eukaryotic chromosomes. Such processes include telomere shortening, telomere extension or conformational changes of telomere DNA through changes in interactions of telomere associated proteins. Here we point out some important features of cell senescence, cell immortalization and factors that are involved in these events.

telomeres; aging

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