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(Received for publication, March 19, 1996, and in revised form, June 10, 1996)
From INSERM U385, Faculté de Médecine, Avenue de
Valombrose, 06107 Nice Cedex 02, France
Ultraviolet B (UVB) radiation is the main
physiological stimulus for human skin pigmentation; however, the
molecular mechanisms underlying this process are still unclear.
Recently, nitric oxide (NO) and cGMP have been involved in mediation of
skin erythema induced by UVB. Therefore, we investigated the role of NO
and cGMP in UVB-induced melanogenesis. In this study, we demonstrated
that UVB stimulation of melanogenesis was mimicked by exogenous NO
donors. Additionally, we showed that NO stimulated cGMP synthesis and
that cGMP was also a potent stimulator of melanogenesis. Furthermore,
the inhibition of the melanogenic effect of NO by guanylate cyclase
inhibitor demonstrated that NO mediated its effect through the
activation of guanylyl cyclase. Interestingly, 1 min after UVB
irradiation, we observed a significant increase in cGMP content in
melanocytes. The effects of UVB on cGMP production and on melanogenesis
were blocked by both guanylate cyclase and NO synthase inhibitors.
Additionally, inhibition of cGMP-dependent kinase also
prevented the stimulation of melanogenesis by UVB and NO. Therefore, we
concluded that NO and cGMP production is required for UVB-induced
melanogenesis and that cGMP mediated its melanogenic effects mainly
through the activation of cGMP-dependent kinase.
Volume 271, Number 45,
Issue of November 8, 1996
pp. 28052-28056
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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