{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T07:03:58Z","timestamp":1771657438253,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,9,25]],"date-time":"2007-09-25T00:00:00Z","timestamp":1190678400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Induction of the p21<jats:sup>WAF1<\/jats:sup> protein (hereafter called p21) following genotoxic stress is known to inhibit proliferating cell nuclear antigen (PCNA)\u2010dependent DNA repair, downregulate apoptosis, and trigger a sustained growth\u2010arrested phenotype called accelerated senescence. Studies with immortalized human and murine cell lines have revealed that exposure to ultraviolet light (UVC; 254 nm) results in the degradation of p21 to facilitate DNA repair and promote cell survival, or may lead to apoptotic cell death. The objective of the present study was to determine whether exposure of non\u2010transformed human fibroblast strains to relatively low fluences of UVC (i.e., fluences typically used in the clonogenic survival assay) might induce sustained nuclear accumulation of p21, leading to accelerated senescence. We have evaluated the responses of normal human fibroblast (NHF) strains and nucleotide excision repair (NER)\u2010deficient fibroblast strains representing xeroderma pigmentosum (XP) complementation groups A and G and Cockayne syndrome (CS) complementation groups A and B. We report that exposure of NHFs to \u226415 J\/m<jats:sup>2<\/jats:sup> of UVC, and NER\u2010deficient fibroblasts to \u22645 J\/m<jats:sup>2<\/jats:sup> of UVC, results in sustained nuclear accumulation of p21 and growth arrest through accelerated senescence. With each fibroblast strain examined, exposure to UVC fluences that resulted in \u223c90% loss of clonogenic potential triggered significant (&gt;60%) accelerated senescence, but only marginal (&lt;5%) apoptosis. We conclude that nuclear accumulation of p21 accompanied by accelerated senescence may be an integral component of the response of human fibroblasts to UVC\u2010induced DNA damage, irrespective of their DNA repair capabilities. J. Cell. Physiol. 215: 55\u201367, 2008. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.21284","type":"journal-article","created":{"date-parts":[[2007,9,25]],"date-time":"2007-09-25T23:19:40Z","timestamp":1190762380000},"page":"55-67","source":"Crossref","is-referenced-by-count":20,"title":["Ultraviolet light exposure triggers nuclear accumulation of p21<sup>WAF1<\/sup> and accelerated senescence in human normal and nucleotide excision repair\u2010deficient fibroblast 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