Research Article

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

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Science  16 Jan 1998:
Vol. 279, Issue 5349, pp. 349-352
DOI: 10.1126/science.279.5349.349

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Abstract

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 foreskin 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 β-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.

  • * These authors contributed equally to this work.

  • To whom correspondence should be addressed. E-mail: slichtste{at}geron.com; wright{at}utsw.swmed.edu

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