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首页> 外文期刊>Journal of Cellular Physiology >STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells
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STIM-1 and ORAI-1 channel mediate angiotensin-II-induced expression of Egr-1 in vascular smooth muscle cells

机译：STIM-1和ORAI-1通道进行调解angiotensin-II-induced Egr-1的表达式血管平滑肌细胞

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An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II) is a key vasoactive peptide that has been implicated in the pathogenesis of vascular diseases. Ang-II elevates intracellular Ca2+ through activation of the store-operated calcium entry (SOCE) involving an inositol-3-phosphate receptor (IP3R)-coupled depletion of endoplasmic reticular Ca2+ and a subsequent activation of the stromal interaction molecule 1 (STIM-1)/Orai-1 complex. However, the involvement of IP3R/STIM-1/Orai-1-Ca2+-dependent signaling in Egr-1 expression in VSMC remains unexplored. Therefore, in the present studies, we have examined the role of Ca2+ signaling in Ang-II-induced Egr-1 expression in VSMC and investigated the contribution of STIM-1 or Orai-1 in mediating this response. 2-aminoethoxydiphenyl borate (2-APB), a dual non-competitive antagonist of IP3R and inhibitor of SOCE, decreased Ang-II-induced Ca2+ release and attenuated Ang-II-induced enhanced expression of Egr-1 protein and mRNA levels. Egr-1 upregulation was also suppressed following blockade of calmodulin and CaMKII. Furthermore, RNA interference-mediated depletion of STIM-1 or Orai-1 attenuated Ang-II-induced Egr-1 expression as well as Ang-II-induced phosphorylation of ERK1/2 and CREB. In addition, siRNA-induced silencing of CREB resulted in a reduction in the expression of Egr-1 stimulated by Ang-II. In summary, our data demonstrate that Ang-II-induced Egr-1 expression is mediated by STIM-1/Orai-1/Ca2+-dependent signaling pathways in A-10 VSMC.
机译：的upregulation Egr-1表达式在动脉粥样硬化模型和内膜的报道增生,各种血管活性的肽和经济增长促进刺激已被证明诱导的表达Egr-1血管平滑肌肉细胞(VSMC)。重要的血管活性肽作用已被牵连血管疾病的发病机理。提升通过激活细胞内的钙离子(跌倒)涉及门店钙条目一个inositol-3-phosphate受体(IP3R)耦合损耗内质的网状Ca2 +的随后激活基质的相互作用分子1 (STIM-1) / Orai-1复杂。参与IP3R / STIM-1 Orai-1-Ca2 +端依赖信号在VSMC Egr-1表达式仍然存在未知的。检查Ca2 +信号的作用吗Ang-II-induced Egr-1 VSMC和表达式调查的贡献STIM-1或Orai-1在调解这种反应。硼酸(2-APB),双非竞争性拮抗剂IP3R和跌倒的抑制剂,减少Ang-II-induced Ca2 +释放和减毒Ang-II-induced增强Egr-1的表情蛋白质和mRNA水平。也抑制钙调蛋白的封锁和CaMKII。interference-mediated STIM-1或损耗Orai-1减毒Ang-II-induced Egr-1表达式以及Ang-II-induced磷酸化ERK1/2和分子。沉默的分子导致减少表达式Ang-II Egr-1刺激的。总结,我们的数据表明Ang-II-inducedEgr-1表达式是由STIM-1 / Orai-1 / Ca2 +端依赖的信号通路在a - 10 VSMC。

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