The gene expression profile of psoralen plus UVA-induced premature senescence in skin fibroblasts resembles a combined DNA-damage and stress-induced cellular senescence response phenotype

C. Borlon, F. Debacq-Chainiaux, O. Toussaint, C. Hinrichs, K. Scharffetter-Kochanek, M. Wlaschek

Research output: Contribution to journalArticlepeer-review

Abstract

After a finite number of population doublings, normal human cells undergo replicative senescence accompanied by growth arrest. We previously described a model of stress-induced premature senescence by treatment of dermal fibroblasts with psoralen plus UVA, a common photodermatological therapy. Psoralen photoactivation has long been used as a therapy for hyperproliferative skin disorders. The repetitive therapeutical treatment is accompanied by premature aging of the skin. Treatment of fibroblasts in vitro with 8-methoxypsoralen (8-MOP) and subsequent ultraviolet A (UVA) irradiation results in growth arrest with morphological and functional changes reminiscent of replicative senescence. For gene expression profiling in two strains of human skin fibroblasts after PUVA treatment, we used a low-density DNA array representing 240 genes involved in senescence and stress response. Twenty-nine genes were differentially expressed after PUVA treatment in the two strains of human skin fibroblasts. These genes are involved in growth arrest, stress response, modification of the extracellular matrix and senescence. This study contributes further to the elucidation of the PUVA model and its validation as a useful stress-induced premature senescence model aiming to characterize the premature senescence of fibroblasts and to identify biomarkers that could be applied in vivo.
Original languageEnglish
Pages (from-to)911-923
Number of pages13
JournalExperimental Gerontology
Volume42
Issue number9
DOIs
Publication statusPublished - 1 Sep 2007

Fingerprint

Dive into the research topics of 'The gene expression profile of psoralen plus UVA-induced premature senescence in skin fibroblasts resembles a combined DNA-damage and stress-induced cellular senescence response phenotype'. Together they form a unique fingerprint.

Cite this