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Repeated Exposures to UVB Induce Differentiation Rather Than Senescence of Human Keratinocytes Lacking p16(INK-4A)

Repeated Exposures to UVB Induce Differentiation Rather Than Senescence of Human Keratinocytes Lacking p16(INK-4A)

Véronique Bertrand-Vallery, Emmanuelle Boilan, Noëlle Ninane, Catherine Demazy, Bertrand Friguet, Olivier Toussaint, Yves Poumay, Florence Debacq-Chainiaux

Biogerontology. 2010 Apr;11(2):167-81.

PMID: 19554468

Abstract:

Skin cancers and extrinsic aging are delayed consequences of cumulative UV radiation insults. Exposure of human keratinocytes to UVB has been previously shown to trigger premature senescence. In order to explore the involvement of the cyclin-dependent kinase inhibitor p16(INK-4a) in UVB-induced premature senescence, we developed an original model of repeated sublethal exposures of human keratinocytes deficient in p16(INK-4a). We did not observe any significant increase of senescence-associated beta-galactosidase activity positive cells following UVB exposure in this cell line in contrast to primary keratinocytes, suggesting a role for p16(INK-4a) in UVB-induced senescence. However, we detected sustained DNA damage, prolonged cell cycle arrest, and induction of markers of epidermal differentiation like involucrin and filaggrin as consequences of the repeated exposures. Keratinocytes exposed to the same dose of UVB in a single exposure died. Furthermore, the abundance of the keratins 6, 16 and 17 was increased in keratinocytes exposed repeatedly to UVB suggesting an alternative differentiation. This model allows the induction of a state of differentiation observed in vivo with differentiation uncoupled from premature senescence.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42415344	p16-INK-4a human			Price

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