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首页> 外文期刊>Journal of cellular physiology. >A novel role of SIRT2 in regulating gap junction communications via connexin-43 in bovine cumulus-oocyte complexes
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A novel role of SIRT2 in regulating gap junction communications via connexin-43 in bovine cumulus-oocyte complexes

机译：一本小说SIRT2调节缝隙连接的作用通信通过connexin-43牛cumulus-oocyte复合物

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摘要

SIRT2, the predominantly cytosolic sirtuin, plays important role in multiple biological processes, including metabolism, stress response, and aging. However, the function of SIRT2 in gap junction intercellular communications (GJICs) of cumulus-oocyte complexes (COCs) is not yet known. The purpose of the present study was to evaluate the effect and underlining mechanism of SIRT2 on GJICs in COCs. Here, we found that treatment with SIRT2 inhibitors (SirReal2 or TM) inhibited bovine oocyte nuclear maturation. Further analysis revealed that SIRT2 inactivation disturbed the GJICs of COCs during in vitro maturation. Correspondingly, both the Cx43 phosphorylation levels and MEK/MER signaling pathways were induced by SIRT2 inhibition. Importantly, SIRT2-mediated Cx43 phosphorylation was completely abolished by treatment with MEK1/2 inhibitor (Trametinib). Furthermore, treatment with SIRT2 inhibitors resulted in the high levels of MEK1/2 acetylation. Functionally, downregulating the MER/ERK pathways with inhibitors (Trametinib or SCH772984) could attenuate the closure of GJICs caused by SIRT2 inactivation in partly. In addition, inhibition of SIRT2 activity significantly decreased the membrane and zona pellucida localization of Cx43 by upregulating the levels of Cx43 acetylation. Taken together, these results demonstrated a novel role that SIRT2 regulates GJICs via modulating the phosphorylation and deacetylation of Cx43 in COCs.
机译：SIRT2,主要是胞质sirtuin蛋白,玩多个生物过程的重要作用,包括代谢、应激反应和老化。然而,SIRT2在缝隙连接的功能细胞间通讯(GJICs)cumulus-oocyte复合物(COCs)还不知道。本研究的目的是评估SIRT2和强调机制的影响COCs GJICs。SIRT2抑制剂(SirReal2或TM)抑制牛卵母细胞的核成熟。分析显示,SIRT2失活不安的GJICs COCs在体外成熟。磷酸化水平和MEK / MER信号通路被SIRT2抑制诱导。重要的是,SIRT2-mediated Cx43磷酸化完全废除MEK1/2治疗抑制剂(Trametinib)。SIRT2抑制剂导致的高水平的MEK1/2乙酰化作用。表达下调MER / ERK途径抑制剂(Trametinib或SCH772984)减弱的关闭GJICs SIRT2所致在部分失活。SIRT2活动明显减少了膜和透明带Cx43的本地化通过上调Cx43乙酰化的水平。综上所述,这些研究结果展示了小说角色SIRT2调节GJICs通过调制磷酸化和脱乙酰作用COCs Cx43。

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