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- Title
Extension of life-span by introduction of telomerase into normal human cells.
- Authors
Bodnar, A G; Ouellette, M; Frolkis, M; Holt, S E; Chiu, C P; Morin, G B; Harley, C B; Shay, J W; Lichtsteiner, S; Wright, W E
- 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 straining for beta-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.
- Publication
Science (New York, N.Y.), 1998, Vol 279, Issue 5349, p349
- ISSN
0036-8075
- Publication type
Journal Article
- DOI
10.1126/science.279.5349.349