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Research Article Free access | 10.1172/JCI119206

Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis.

C Roméro-Graillet, E Aberdam, M Clément, J P Ortonne, and R Ballotti

Institut National de la Santé et de la Recherche Médicale U385, Faculté de Médecine, Nice, France. romero@unice.fr

Find articles by Roméro-Graillet, C. in: JCI | PubMed | Google Scholar

Institut National de la Santé et de la Recherche Médicale U385, Faculté de Médecine, Nice, France. romero@unice.fr

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Institut National de la Santé et de la Recherche Médicale U385, Faculté de Médecine, Nice, France. romero@unice.fr

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Institut National de la Santé et de la Recherche Médicale U385, Faculté de Médecine, Nice, France. romero@unice.fr

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Institut National de la Santé et de la Recherche Médicale U385, Faculté de Médecine, Nice, France. romero@unice.fr

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Published February 15, 1997 - More info

Published in Volume 99, Issue 4 on February 15, 1997
J Clin Invest. 1997;99(4):635–642. https://doi.org/10.1172/JCI119206.
© 1997 The American Society for Clinical Investigation
Published February 15, 1997 - Version history
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Abstract

Ultraviolet (UV) radiation is the main physiological stimulus for human skin pigmentation. Within the epidermal-melanin unit, melanocytes synthesize and transfer melanin to the surrounding keratinocytes. Keratinocytes produce paracrine factors that affect melanocyte proliferation, dendricity, and melanin synthesis. In this report, we show that normal human keratinocytes secrete nitric oxide (NO) in response to UVA and UVB radiation, and we demonstrate that the constitutive isoform of keratinocyte NO synthase is involved in this process. Next, we investigate the melanogenic effect of NO produced by keratinocytes in response to UV radiation using melanocyte and keratinocyte cocultures. Conditioned media from UV-exposed keratinocytes stimulate tyrosinase activity of melanocytes. This effect is reversed by NO scavengers, suggesting an important role for NO in UV-induced melanogenesis. Moreover, melanocytes respond to NO-donors by decreased growth, enhanced dendricity, and melanogenesis. The rise in melanogenesis induced by NO-generating compounds is associated with an increased amount of both tyrosinase and tyrosinase-related protein 1. These observations suggest that NO plays an important role in the paracrine mediation of UV-induced melanogenesis.

Version history
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