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Extension of Life-Span by Introduction of Telomerase into Normal                                           Human Cells


Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state
called replicative senescence. It has been proposed that telomere shortening is the molecular clock
that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types,
retinal pigment epithelial cells and fore-skin fibroblasts, were transfected with vectors encoding the
human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which
exhibited telomere shortening and senescence, telomerase-expressing clones had elongated
telomeres, divided vigorously, and showed reduced staining for b-galactosidase, a biomarker for
senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already
exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship
between telomere shortening and in vitro cellular senescence. The ability to maintain normal human
cells in a phenotypically youthful state could have important applications in research and medicine.

 
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