GNA12 regulates C5a-induced migration by downregulating C5aR1-PLCβ2-PI3K-AKT-ERK1/2 signaling.

Haonan Yu, Zhihua Liu
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Abstract

Gna12 has been identified as one of the reported inflammatory bowel disease (IBD) susceptibility genes in genome-wide association studies (GWAS). However, the function of GNA12 in intestinal homeostasis remains unknown. Here we report that GNA12, a G-protein α subunit, regulates C5a-induced migration in macrophages. Deficiency of GNA12 results in enhanced migration induced by C5a in macrophages. Mechanistically, GNA12 suppresses C5a-induced migration by downregulating the C5aR1-PLCβ2-PI3K-AKT-ERK1/2 signaling. Therefore, our study reveals that GNA12 is an anti-inflammatory factor, which might alleviate the development of inflammation by inhibiting the excessive chemotactic migration of macrophages.

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GNA12通过下调c5ar1 - plc - β2- pi3k - akt - erk1 /2信号通路调控c5a诱导的迁移。
在全基因组关联研究(GWAS)中,Gna12已被确定为报道的炎症性肠病(IBD)易感基因之一。然而,GNA12在肠道内稳态中的功能尚不清楚。在这里,我们报道了GNA12,一个g蛋白α亚基,调节c5a诱导的巨噬细胞迁移。GNA12缺乏导致巨噬细胞在C5a诱导下迁移增强。从机制上讲,GNA12通过下调c5ar1 - plc - β2- pi3k - akt - erk1 /2信号通路抑制c5a诱导的迁移。因此,我们的研究揭示了GNA12是一种抗炎因子,可能通过抑制巨噬细胞过度趋化迁移来缓解炎症的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
1.30
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117
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