Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin

Hu, Bang-li, Shi, Cheng, Lei, Rong-e, Lu, Dong-hong, Luo, Wei, Qin, Shan-yu, Zhou, You ORCID: https://orcid.org/0000-0002-1743-1291 and Jiang, Hai-xing 2016. Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin. Scientific Reports 6 , 36436. 10.1038/srep36436

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Abstract

IL-22 ameliorates liver fibrosis by inhibiting hepatic stellate cells (HSC), and loss of miR-200a is associated with the development of liver fibrosis. The study aimed to investigate the interplay between IL-22 and miR-200a in regulating liver fibrosis in vivo and in vitro. We observed that IL-22 significantly reduced the proliferation of HSC and increased the expression of p-STAT3. β-catenin was identified as a target gene of miR-200a by luciferase reporter assay, and upregulation of miR-200a significantly attenuated the proliferation of HSC and reduced β-catenin expression. IL-22 treatment increased expression of miR-200a and decreased expression of β-catenin in HSC. The expression of p-STAT3 and miR-200a was elevated while β-catenin was decreased in fibrotic rat liver after IL-22 treatment. Expression levels of β-catenin and p-STAT3 were inversely correlated in fibrotic rat liver and HSC. Upregulation of β-catenin suppressed expression of p-STAT3 in HSC. We concluded that IL-22 inhibits HSC activation and ameliorates liver fibrosis through enhancing expression of miR-200a and reducing expression of β-catenin, suggesting there may be a crosstalk between IL-22/STAT3 and β-catenin pathway.

Item Type:	Article
Date Type:	Published Online
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI)
Subjects:	R Medicine > R Medicine (General)
Uncontrolled Keywords:	Interleukins Liver fibrosis
Publisher:	Nature Publishing Group
ISSN:	2045-2322
Date of First Compliant Deposit:	28 December 2016
Date of Acceptance:	17 October 2016
Last Modified:	04 May 2023 19:51
URI:	https://orca.cardiff.ac.uk/id/eprint/97110

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