2009
DOI: 10.2353/ajpath.2009.080332
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Senescent Keratinocytes Die by Autophagic Programmed Cell Death

Abstract: Normal cells reach senescence after a specific time and number of divisions, leading ultimately to cell death. Although escape from this fate may be a requisite step in neoplastic transformation, the mechanisms governing senescent cell death have not been well investigated. We show here, using normal human epidermal keratinocytes, that no apoptotic markers appear with senescence. In contrast, the expression of several proteins involved in the regulation of macroautophagy, notably Beclin-1 and Bcl-2, was found … Show more

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Cited by 105 publications
(98 citation statements)
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“…Several reports have recently described the autophagy process occurring in monolayer cultures of keratinocytes (Aymard et al, 2011;Chatterjea et al, 2011;Deruy et al, 2010;Gosselin et al, 2009;Lee et al, 2011;Silva et al, 2010;Tong et al, 2012;Wang and Levine, 2011;Zhao et al, 2013;Zhou and Münger, 2009). Autophagy is a highly conserved proteolytic mechanism that maintains the homeostasis of the cell by degrading organelles and cytoplasmic material.…”
Section: Introductionmentioning
confidence: 99%
“…Several reports have recently described the autophagy process occurring in monolayer cultures of keratinocytes (Aymard et al, 2011;Chatterjea et al, 2011;Deruy et al, 2010;Gosselin et al, 2009;Lee et al, 2011;Silva et al, 2010;Tong et al, 2012;Wang and Levine, 2011;Zhao et al, 2013;Zhou and Münger, 2009). Autophagy is a highly conserved proteolytic mechanism that maintains the homeostasis of the cell by degrading organelles and cytoplasmic material.…”
Section: Introductionmentioning
confidence: 99%
“…105 A third study demonstrated that senescent keratinocytes seem to die through massive and specific autophagic degradation of their nuclei and mitochondria, although degradation of other cellular organelles was not examined. 106 Other findings supported the role of autophagy in the death of senescent keratinocytes. The autophagy inhibitor 3-methyladenine can delay the death of senescent cells.…”
Section: Autophagic Degradation Of the Nucleus And Its Components Insupporting
confidence: 55%
“…This notion was supported by the altered morphology of the nuclei and mitochondria within the central domain and by the level of DNA degradation observed. 106 It is possible that the nuclei of senescent cells in general could be targeted for autophagy simply because their DNA is damaged, since inhibition of DNA-protein kinase, a nuclear kinase involved in DNA-break signaling, sensitizes to autophagy in malignant glioma cells, 107 suggesting that persistence of damaged DNA can activate the autophagic process. Similarly, both an increase in Beclin-1 (mammalian homologue of Atg6p) expression and a concomitant increase in autophagic activity occur following treatment with the DNA-damaging agent etoposide.…”
Section: A Second Form Of Autophagic Degradation Of the Yeast Nucleusmentioning
confidence: 99%
“…Both in vitro and in vivo, as a result of time and cumulative divisions, normal cells enter senescence, characterized by an enlarged morphology, lipofuscin accumulation, increased autophagic activity, cell cycle arrest, and frequent polynucleation (1)(2)(3)(4)(5). It is accepted that senescence results from cumulative oxidative damage and telomere shortening, each probably acting to a different degree according to cell type or environmental conditions.…”
Section: Introductionmentioning
confidence: 99%