Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

Ruben D. Ramirez; Carmela P. Morales; Brittney Shea Herbert; Jeffrey M. Rohde; Christina Passons; Jerry W. Shay; Woodring E. Wright

doi:10.1101/gad.859201

Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

Ruben D. Ramirez, Carmela P. Morales, Brittney Shea Herbert, Jeffrey M. Rohde, Christina Passons, Jerry W. Shay, Woodring E. Wright

Research output: Contribution to journal › Article › peer-review

397 Scopus citations

Abstract

Telomere shortening is the mechanism underlying replicative aging in fibroblasts. A variety of reports now claim that inactivation of the p16^1NK4a/pRB pathway is required in addition to telomere maintenance for the immortalization of cells such as skin keratinocytes and breast epithelial cells. We here show that the premature growth arrest of these cell types can be explained by an inadequate culture environment. Providing mesenchymal/epithelial interactions by cultivating the telomerase-expressing cells on feeder layers avoids the growth arrest associated with increased p16^1NK4a. These results do not support a telomere-independent mechanism of replicative aging.

Original language	English (US)
Pages (from-to)	398-403
Number of pages	6
Journal	Genes and Development
Volume	15
Issue number	4
DOIs	https://doi.org/10.1101/gad.859201
State	Published - 2001

Keywords

Aging
Cancer
Cellular senescence
P16
Replicative aging
Telomeres

ASJC Scopus subject areas

Genetics
Developmental Biology

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10.1101/gad.859201

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title = "Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions",

abstract = "Telomere shortening is the mechanism underlying replicative aging in fibroblasts. A variety of reports now claim that inactivation of the p161NK4a/pRB pathway is required in addition to telomere maintenance for the immortalization of cells such as skin keratinocytes and breast epithelial cells. We here show that the premature growth arrest of these cell types can be explained by an inadequate culture environment. Providing mesenchymal/epithelial interactions by cultivating the telomerase-expressing cells on feeder layers avoids the growth arrest associated with increased p161NK4a. These results do not support a telomere-independent mechanism of replicative aging.",

keywords = "Aging, Cancer, Cellular senescence, P16, Replicative aging, Telomeres",

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AU - Ramirez, Ruben D.

AU - Morales, Carmela P.

AU - Herbert, Brittney Shea

AU - Rohde, Jeffrey M.

AU - Passons, Christina

AU - Shay, Jerry W.

AU - Wright, Woodring E.

PY - 2001

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N2 - Telomere shortening is the mechanism underlying replicative aging in fibroblasts. A variety of reports now claim that inactivation of the p161NK4a/pRB pathway is required in addition to telomere maintenance for the immortalization of cells such as skin keratinocytes and breast epithelial cells. We here show that the premature growth arrest of these cell types can be explained by an inadequate culture environment. Providing mesenchymal/epithelial interactions by cultivating the telomerase-expressing cells on feeder layers avoids the growth arrest associated with increased p161NK4a. These results do not support a telomere-independent mechanism of replicative aging.

AB - Telomere shortening is the mechanism underlying replicative aging in fibroblasts. A variety of reports now claim that inactivation of the p161NK4a/pRB pathway is required in addition to telomere maintenance for the immortalization of cells such as skin keratinocytes and breast epithelial cells. We here show that the premature growth arrest of these cell types can be explained by an inadequate culture environment. Providing mesenchymal/epithelial interactions by cultivating the telomerase-expressing cells on feeder layers avoids the growth arrest associated with increased p161NK4a. These results do not support a telomere-independent mechanism of replicative aging.

KW - Aging

KW - Cancer

KW - Cellular senescence

KW - P16

KW - Replicative aging

KW - Telomeres

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Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

Abstract

Keywords

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