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 journalArticle

370 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)398-403
Number of pages6
JournalGenes and Development
Volume15
Issue number4
DOIs
StatePublished - 2001

Fingerprint

Telomere
Telomere Shortening
Feeder Cells
Telomerase
Growth
Keratinocytes
Breast
Fibroblasts
Epithelial Cells
Maintenance
Skin

Keywords

  • Aging
  • Cancer
  • Cellular senescence
  • P16
  • Replicative aging
  • Telomeres

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

Cite this

Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions. / Ramirez, Ruben D.; Morales, Carmela P.; Herbert, Brittney Shea; Rohde, Jeffrey M.; Passons, Christina; Shay, Jerry W.; Wright, Woodring E.

In: Genes and Development, Vol. 15, No. 4, 2001, p. 398-403.

Research output: Contribution to journalArticle

Ramirez, Ruben D. ; Morales, Carmela P. ; Herbert, Brittney Shea ; Rohde, Jeffrey M. ; Passons, Christina ; Shay, Jerry W. ; Wright, Woodring E. / Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions. In: Genes and Development. 2001 ; Vol. 15, No. 4. pp. 398-403.
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