Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice
Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice
复制标题
胰岛细胞自身抗原 69 通过下调 Tgfbr1 和减弱小鼠 Tgf beta 信号传导加速肝脏再生
DOI：
10.1002/1873-3468.13859
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发表时间：
2020-07-17
期刊：
影响因子：
3.5
通讯作者：
Lyu, Jianxin
中科院分区：
文献类型：
--
作者：
Chen, Linjie;Tao, Fei;Lyu, Jianxin
再生是肝组织对毒性化学物质或手术切除引起的功能性细胞损失的独特防御机制。在这项研究中，我们发现胰岛细胞自身抗原69（Ica69）加速小鼠的肝再生。在70%部分肝切除后，Ica69 mRNA和蛋白在小鼠肝细胞中在肝再生的早期阶段显著上调。与野生型小鼠相比，Ica69缺陷小鼠肝切除术后肝损伤更严重，肝再生延迟，手术意外死亡率更高。在机制上，Ica69与Pick1蛋白相互作用以调节Tgfbr 1蛋白表达和Tgf β诱导的Smad2磷酸化。我们的研究结果表明，肝组织中的Ica69是促进肝再生的新的潜在靶点。
Regeneration is a unique defense mechanism of liver tissue in response to functional cell loss induced by toxic chemicals or surgical resection. In this study, we found that Islet-cell autoantigen 69 (Ica69) accelerates liver regeneration in mice. Following 70% partial hepatectomy, both Ica69 mRNA and protein are significantly upregulated in mouse hepatocytes at the early stage of liver regeneration. Compared with the wild-type mice, Ica69-deficient mice have more severe liver injury, delayed liver regeneration, and high surgical accidental mortality following hepatectomy. Mechanistically, Ica69 interacts with Pick1 protein to regulate Tgfbr1 protein expression and Tgf beta-induced Smad2 phosphorylation. Our findings suggest that Ica69 in liver tissue is a new potential target for promoting liver regeneration.