Aging of human cells can be reproduced in monolayer cultures, revealing the phenotype of replicative senescence. It was shown that diploid human fibroblasts enter a stable growth arrest phenotype at the end of their lifespan and, in particular, these cells are resistant to various apoptotic stimuli. In contrast, human endothelial cells from the umbilical vein (HUVEC) acquire a proapoptotic phenotype when reaching senescence and this probably results from reactive oxygen species (ROS) induced damage and associated signaling. Ceramides were shown to accumulate in senescent fibroblasts and are also known as potent regulators of apoptotic cell death. To further study age-associated changes in proneness to apoptosis between fibroblasts and endothelial cells, both cell types were challenged by administration of exogenous ceramide and apoptotic cell death was determined. While ceramide can efficiently induce apoptosis in both young and senescent cells of either histotype, quantitative evaluation of the data show that senescent fibroblasts are more resistant to apoptosis induction when compared to their young counterparts, whereas in the case of endothelial cells proneness for apoptosis is increased in senescent cells. Together, these data suggest significant differences in the regulation of apoptosis associated with senescence in fibroblasts and endothelial cells. © 2004 Elsevier Inc. All rights reserved.

Hampel, B., Malisan, F., Niederegger, H., Testi, R., Jansen Durr, P. (2004). Differential regulation of apoptotic cell death in senescent human cells. In Experimental Gerontology (pp.1713-1721) [10.1016/j.exger.2004.05.010].

Differential regulation of apoptotic cell death in senescent human cells

MALISAN, FLORENCE;TESTI, ROBERTO;
2004-01-01

Abstract

Aging of human cells can be reproduced in monolayer cultures, revealing the phenotype of replicative senescence. It was shown that diploid human fibroblasts enter a stable growth arrest phenotype at the end of their lifespan and, in particular, these cells are resistant to various apoptotic stimuli. In contrast, human endothelial cells from the umbilical vein (HUVEC) acquire a proapoptotic phenotype when reaching senescence and this probably results from reactive oxygen species (ROS) induced damage and associated signaling. Ceramides were shown to accumulate in senescent fibroblasts and are also known as potent regulators of apoptotic cell death. To further study age-associated changes in proneness to apoptosis between fibroblasts and endothelial cells, both cell types were challenged by administration of exogenous ceramide and apoptotic cell death was determined. While ceramide can efficiently induce apoptosis in both young and senescent cells of either histotype, quantitative evaluation of the data show that senescent fibroblasts are more resistant to apoptosis induction when compared to their young counterparts, whereas in the case of endothelial cells proneness for apoptosis is increased in senescent cells. Together, these data suggest significant differences in the regulation of apoptosis associated with senescence in fibroblasts and endothelial cells. © 2004 Elsevier Inc. All rights reserved.
7th International Symposium on the Neurobiology and Neuroendocrinology of Aging
Bregenz, AUSTRIA
JUL 18-23, 2004
Rilevanza internazionale
2004
Settore MED/04 - PATOLOGIA GENERALE
English
Apoptosis; Ceramides; Endothelial cells; Fibroblasts; Human aging; Senescence
Intervento a convegno
Hampel, B., Malisan, F., Niederegger, H., Testi, R., Jansen Durr, P. (2004). Differential regulation of apoptotic cell death in senescent human cells. In Experimental Gerontology (pp.1713-1721) [10.1016/j.exger.2004.05.010].
Hampel, B; Malisan, F; Niederegger, H; Testi, R; Jansen Durr, P
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/31232
Citazioni
  • ???jsp.display-item.citation.pmc??? 36
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 87
social impact