Islet‐cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice,FEBS Letters

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Islet‐cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice
FEBS Letters ( IF 3.0 ) Pub Date : 2020-07-17 , DOI: 10.1002/1873-3468.13859
Linjie Chen _{1,

2} , Fei Tao ₃ , Yangyang Zhang ₄ , Chongyi Shu ₃ , Weiling Xiang _{1,

2} , Leixiang Yang ₅ , Xiaopan Chen ₅ , Yeting Hong ₁ , Bingyu Chen _{1,

2,

5} , Kaiqiang Li _{1,

2,

5} , Wei Zhang _{2,

5} , Ke Hao _{1,

2,

5} , Feihang Ge _{1,

5} , Zhen Wang _{1,

2,

5} , Jianxin Lyu ₃

Affiliation

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 Tgfβ‐induced Smad2 phosphorylation. Our findings suggest that Ica69 in liver tissue is a new potential target for promoting liver regeneration.

中文翻译：

胰岛细胞自身抗原 69 通过下调 Tgfbr1 和减弱小鼠的 Tgfβ 信号来加速肝脏再生

再生是一种独特的肝脏组织防御机制，以应对有毒化学物质或手术切除引起的功能性细胞损失。在这项研究中，我们发现胰岛细胞自身抗原 69 (Ica69) 可加速小鼠的肝脏再生。70% 部分肝切除后，小鼠肝细胞中 Ica69 mRNA 和蛋白质在肝脏再生的早期均显着上调。与野生型小鼠相比，Ica69 缺陷小鼠在肝切除术后具有更严重的肝损伤、肝再生延迟和高手术意外死亡率。从机制上讲，Ica69 与 Pick1 蛋白相互作用以调节 Tgfbr1 蛋白表达和 Tgfβ 诱导的 Smad2 磷酸化。我们的研究结果表明肝组织中的 Ica69 是促进肝脏再生的新潜在靶点。

更新日期：2020-07-17

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