Premium
Islet‐cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice
Author(s) -
Chen Linjie,
Tao Fei,
Zhang Yangyang,
Shu Chongyi,
Xiang Weiling,
Yang Leixiang,
Chen Xiaopan,
Hong Yeting,
Chen Bingyu,
Li Kaiqiang,
Zhang Wei,
Hao Ke,
Ge Feihang,
Wang Zhen,
Lyu Jianxin
Publication year - 2020
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13859
Subject(s) - liver regeneration , regeneration (biology) , downregulation and upregulation , hepatectomy , islet , liver injury , microbiology and biotechnology , phosphorylation , biology , cancer research , endocrinology , medicine , resection , biochemistry , insulin , surgery , gene
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.