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ORAI1 Ca2+ Channels Control Endothelin-1-Induced Mitogenesis and Melanogenesis in Primary Human Melanocytes

机译:ORaI1 Ca2 +通道控制内皮素-1诱导原代人黑素细胞的有丝分裂和黑素生成

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摘要

UV radiation of the skin triggers keratinocytes to secrete endothelin-1 (ET-1) that binds to endothelin receptorsudon neighboring melanocytes. Melanocytes respond with a prolonged increase in intracellular Ca2þudconcentration ([Ca2þ]i), which is necessary for proliferation and melanogenesis. A major fraction of theudCa2þ signal is caused by entry through Ca2þ-permeable channels of unknown identity in the plasmaudmembrane. ORAI Ca2þ channels are molecular determinants of Ca2þ release-activated Ca2þ (CRAC) channelsudand are expressed in many tissues. Here, we show that ORAI1–3 and their activating partners stromal interactionudmolecules 1 and 2 (STIM1 and STIM2) are expressed in human melanocytes. Although ORAI1 is theudpredominant ORAI isoform, STIM2 mRNA expression exceeds STIM1. Inhibition of ORAI1 by 2-aminoethoxydiphenyludborate (2-APB) or downregulation of ORAI1 by small interfering RNA (siRNA) reduced Ca2þ entry andudCRAC current amplitudes in activated melanocytes. In addition, suppression of ORAI1 caused reduction inudthe ET-1-induced cellular viability, melanin synthesis, and tyrosinase activity. Our results imply a role forudORAI1 channels in skin pigmentation and their potential involvement in UV-induced stress responses of theudhuman skin.
机译:皮肤的紫外线辐射会触发角质形成细胞分泌内皮素-1(ET-1),内皮素-1(ET-1)与内皮素受体或邻近的黑素细胞结合。黑色素细胞的响应是细胞内Ca2 + / ud浓度([Ca2 +] i)的持续增加,这对于增殖和黑色素生成是必不可少的。 udCa2 +信号的主要部分是由血浆/膜中未知身份的Ca2 +渗透通道进入引起的。 ORAI Ca2 +通道是Ca2 +释放激活的Ca2 +(CRAC)通道的分子决定因子,在许多组织中都有表达。在这里,我们显示了ORAI1-3及其激活伙伴基质相互作用核分子1和2(STIM1和STIM2)在人类黑素细胞中表达。尽管ORAI1是主要的ORAI亚型,但STIM2 mRNA表达超过STIM1。 2-氨基乙氧基二苯基 udborate(2-APB)抑制ORAI1或小干扰RNA(siRNA)下调ORAI1降低了活化黑素细胞中Ca2 +进入和udCRAC电流幅度。此外,抑制ORAI1导致ET-1诱导的细胞活力,黑色素合成和酪氨酸酶活性降低。我们的研究结果暗示了 udORAI1通道在皮肤色素沉着中的作用,以及它们可能参与UV诱导的 udhuman皮肤的应激反应。

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