Relationship between donor age and the replicative lifespan of human cells in culture: A reevaluation

Cristofalo, Vincent J.; Allen, Robert G.; Pignolo, Robert J.; Martin, Bernard; Beck, Jeanne C.

doi:10.1073/pnas.95.18.10614

Cited by 504 publications

(298 citation statements)

References 54 publications

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“…On the other hand, however, the concept has been met with some criticism when the study, in which health status of the donors and biopsy conditions were carefully controlled, failed to demonstrate the correlation between replicative lifespan of skin fibroblasts and the donors' age (Cristofalo et al, 1998). We have previously characterized replicative senescence of HPMC in vitro and on this occasion we have observed a borderline negative correlation between HPMC replicative lifespan and the donor's age (Ksiazek et al, 2006).…”

Section: Discussionmentioning

confidence: 95%

Correlation between the donor age and the proliferative lifespan of human peritoneal mesothelial cells in vitro: Is TGF-β1 a link?

Książek¹,

Winckiewicz²,

Staniszewski³

et al. 2007

Experimental Gerontology

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Section: Discussionmentioning

confidence: 95%

Correlation between the donor age and the proliferative lifespan of human peritoneal mesothelial cells in vitro: Is TGF-β1 a link?

Książek¹,

Winckiewicz²,

Staniszewski³

et al. 2007

Experimental Gerontology

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“…As the WS cells were short-lived adult dermal cells, it is possible that the effects seen with SB203580 were due to a combination of an adult dermal cell-specific effect and a short lifespan. As normal human adult dermal fibroblasts have a replicative lifespan ranging from approximately 25 to 70 PDs (Cristofalo et al 1998), it is possible that SB203580 treatment would have a similar effect on short-lived normal cells as is seen for WS cells.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, in this study, we have used four normal adult dermal fibroblast strains that have replicative lifespans ranging from 24 to 48 PDs (Cristofalo et al 1998). The lifespans of the short-lived normal strains are at the upper range of the WS strains (Davis et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, four strains of adult dermal fibroblasts were used in this study that were chosen to have a range of replicative lifespan from 21 to 50 PDs (Cristofalo et al 1998). To assess the effects of treatment of primary adult fibroblasts with SB203580, cells were grown continuously in the presence or absence of the drug until they reached M1 senescence.…”

Section: Effects Of Sb203580 On the Growth Of Normal Adult Dermal Fibmentioning

confidence: 99%

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Assessing the role of stress signalling via p38 MAP kinase in the premature senescence of Ataxia Telangiectasia and Werner syndrome fibroblasts

Davis

Kipling

2008

Biogerontology

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The premature ageing Ataxia Telangiectasia (AT) and Werner syndromes (WS) are associated with accelerated cellular ageing. Young WS fibroblasts have an aged appearance and activated p38 MAP kinase, and treatment with the p38 inhibitor SB230580 extends their lifespan to within the normal range. SB203580 also extends the replicative lifespan of normal adult dermal fibroblasts, however, the effect is much reduced when compared to WS cells, suggesting that WS fibroblasts undergo a form of stress-induced premature senescence (SIPS). A small lifespan extension is seen in AT cells, which is not significant compared to normal fibroblasts, and the majority of young AT cells do not have an aged appearance and lack p38 activation, suggesting that the premature ageing does not result from SIPS. The lack of p38 activation is supported by the clinical manifestation, since AT is not associated with inflammatory disease, whereas WS individuals are predisposed to atherosclerosis, type II diabetes and osteoporosis, conditions known to be associated with p38 activation.

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“…Cell cultures, established from donos with various diseases, including diabetes mellitus, Werner syndrome, Hutchinson Á/Gilford syndrome and Down's syndrome also exhibit decreased proliferative potential [123]. However, it was shown, that if health status and biopsy conditions are well controlled, the replicative senescence of human fibroblasts in culture does not correlate with donor age [129].…”

Section: Cellular Senescence and Carcinogenesismentioning

confidence: 99%

The relationship between aging and carcinogenesis: a critical appraisal

Anisimov

2003

Critical Reviews in Oncology/Hematology

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The incidence of cancer increases with age in humans and in laboratory animals alike. There are different patterns of age-related distribution of tumors in different organs and tissues. Aging may increase or decrease the susceptibility of various tissues to initiation of carcinogenesis and usually facilitates promotion and progression of carcinogenesis. Aging may predispose to cancer by several mechanisms: (1) tissue accumulation of cells in late stages of carcinogenesis; (2) alterations in homeostasis, in particular, alterations in immune and endocrine system and (3) telomere instability linking aging and increased cancer risk. Increased susceptibility to the effects of tumor promoters is found both in aged animals and aged humans, as predicted by the multistage model of carcinogenesis. Available evidence supporting the relevance of replicative senescence of human cells and telomere biology to human cancer seems quite strong, however, the evidence linking cellular senescence to human aging is controversial and required additional stuidies. Data on the acceleration of aging by carcinogenic agents as well as on increased cancer risk in patients with

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Relationship between donor age and the replicative lifespan of human cells in culture: A reevaluation

Cited by 504 publications

References 54 publications

Correlation between the donor age and the proliferative lifespan of human peritoneal mesothelial cells in vitro: Is TGF-β1 a link?

Correlation between the donor age and the proliferative lifespan of human peritoneal mesothelial cells in vitro: Is TGF-β1 a link?

Assessing the role of stress signalling via p38 MAP kinase in the premature senescence of Ataxia Telangiectasia and Werner syndrome fibroblasts

The relationship between aging and carcinogenesis: a critical appraisal

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