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JCS ePress
online publication date 25 Jan 2005
doi: 10.1242/jcs.01651
Research Article
Repeated exposure of human skin fibroblasts to UVB at subcytotoxic level triggers premature senescence through the TGF-
1 signaling pathway
Florence Debacq-Chainiaux,
Céline Borlon,
Thierry Pascal,
Véronique Royer,
François Eliaers,
Noëlle Ninane,
Géraldine Carrard,
Bertrand Friguet,
Françoise de Longueville,
Sophie Boffe,
José Remacle,
and
Olivier Toussaint*
* Author for correspondence (e-mail: olivier.toussaint{at}fundp.ac.be)
Premature senescence of human diploid fibroblasts (HDFs) can be induced by exposures to a variety of oxidative stress and DNA damaging agents. In this study we developed a robust model of UVB-induced premature senescence of skin HDFs. After a series of 10 subcytotoxic (non-proapoptotic) exposures to UVB at 250 mJ/cm2, the so-called biomarkers of senescence were markedly expressed: growth arrest, senescence-associated 
-galactosidase activity, senescence-associated gene overexpression, deletion in mitochondrial DNA. A set of 44 stress- and senescence-associated genes were found to be differentially expressed in this model, among which clusterin/apolipoprotein J (apo J) and transforming growth factor-1 (TGF-1). Transfection of apo J cDNA provided protection against premature senescence-inducing doses of UVB and other stressful agents. Neutralizing antibodies against TGF-1 or its receptor II (TRII) sharply attenuated the senescence-associated features, suggesting a role for TGF-1 in UVB-induced premature senescence. Both the latent and active forms of TGF-1 were increased with time after the last UVB stress. Proteasome inhibition was ruled out as a potential mechanism of UVB-induced stress-induced premature senescence (SIPS). This model represents an alternative in vitro model in photoaging research for screening potential anti-photoaging compounds.
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