Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice.

Linjie Chen, Fei Tao, Yangyang Zhang, Chongyi Shu, Weiling Xiang, Leixiang Yang, Xiaopan Chen, Yeting Hong, Bingyu Chen, Kaiqiang Li, Wei Zhang, Ke Hao, Feihang Ge, Zhen Wang, Jianxin Lyu

FEBS letters 2020 Sep

filter terms:

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. © 2020 Federation of European Biochemical Societies.

Citation

Linjie Chen, Fei Tao, Yangyang Zhang, Chongyi Shu, Weiling Xiang, Leixiang Yang, Xiaopan Chen, Yeting Hong, Bingyu Chen, Kaiqiang Li, Wei Zhang, Ke Hao, Feihang Ge, Zhen Wang, Jianxin Lyu. Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfβ signaling in mice. FEBS letters. 2020 Sep;594(17):2881-2893