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Interleukin 10 protects primary melanocyte by activation of Stat-3 and PI3K/Akt/NF-kappa B signaling pathways

机译:白细胞介素10通过激活Stat-3和PI3K / Akt /NF-κB信号通路来保护原代黑素细胞

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摘要

Vitiligo is a common melanocytopenic disorder of the skin, with acquired focal depigmentation. Normal human skin relies on melanocytes to provide photoprotection and thermoregulation by producing melanin. Interleukin 10 (IL-10) is a pleiotropic immunoregulatory cytokine drawing more and more researchers' attention. The present study was conducted to investigate the effects of IL-10 on melanocytes and elucidate the underlying mechanisms. We proved that IL-10 play no role in regulating melanogenesis of normal human foreskin-derived epidermal melanocytes (NHEM). IL-10 stimulation activated the JAK/Stat-3 and PI3K/Akt signaling pathways. Moreover, IL-10 treatment increased translocation of p65 NF-icB into the nuclear compartment, and up -regulated expression of the pro-survival proteins Bcl-2 and Bcl-xL. IL-10 restored anti-apoptotic proteins expression and suppressed cytochrome c release in H2O2-induced apoptosis. In conclusion, IL-10 may provide pro-survival cues to melanocytes and be applied in the treatment of vitiligo and other depigmenting disorders. (C) 2016 Elsevier Ltd. All rights reserved.
机译:白癜风是皮肤常见的黑素细胞减少症,伴有局灶性色素沉着。正常人的皮肤依靠黑色素细胞产生黑色素来提供光保护和温度调节。白细胞介素10(IL-10)是一种多效性免疫调节细胞因子,受到越来越多研究人员的关注。进行本研究以研究IL-10对黑素细胞的影响并阐明其潜在机制。我们证明,IL-10在调节正常人包皮衍生的表皮黑素细胞(NHEM)的黑素生成中没有作用。 IL-10刺激激活了JAK / Stat-3和PI3K / Akt信号通路。此外,IL-10处理增加了p65 NF-icB进入核区室的转运,并上调了生存蛋白Bcl-2和Bcl-xL的表达。 IL-10在H2O2诱导的细胞凋亡中恢复了抗凋亡蛋白的表达并抑制了细胞色素c的释放。总之,IL-10可能为黑素细胞提供生存前提示,并可以用于治疗白癜风和其他色素沉着疾病。 (C)2016 Elsevier Ltd.保留所有权利。

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