Ultraviolet B radiation acts through the nitric oxide and cGMP signal transduction pathway to stimulate melanogenesis in human melanocytes
Ultraviolet B radiation acts through the nitric oxide and cGMP signal transduction pathway to stimulate melanogenesis in human melanocytes
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DOI：
10.1074/jbc.271.45.28052
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发表时间：
1996-11-08
影响因子：
4.8
通讯作者：
Ballotti, R
中科院分区：
文献类型：
--
作者：
RomeroGraillet, C;Aberdam, E;Ballotti, R
紫外线B（UVB）辐射是人体皮肤色素沉着的主要生理刺激；然而，这一过程背后的分子机制仍不清楚。最近，一氧化氮 (NO) 和 cGMP 参与了 UVB 引起的皮肤红斑的调节。因此，我们研究了 NO 和 cGMP 在 UVB 诱导的黑素生成中的作用。在这项研究中，我们证明外源性 NO 供体可以模仿 UVB 刺激黑素生成。此外，我还发现，NO 刺激 cGMP 合成，并且 cGMP 也是黑素生成的有效刺激剂。此外，鸟苷酸环化酶抑制剂对 NO 黑素生成作用的抑制表明，NO 通过激活鸟苷酸环化酶来介导其作用。有趣的是，WE照射后1分钟，我们观察到黑素细胞中cGMP含量显着增加。 UVB 对 cGMP 产生和黑素生成的影响被鸟苷酸环化酶和 NO 合酶抑制剂阻断。此外，抑制 cGMP 依赖性激酶还可阻止 UVB 和 NO 刺激黑素生成。因此，我们得出结论，NO和cGMP的产生是UVB诱导的黑素生成所必需的，并且cGMP主要通过cGMP依赖性激酶的激活来介导其黑素生成作用。
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, me 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 WE 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.