Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin.
Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin.
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Interleukin-22 通过 miR-200a/β-catenin 改善肝纤维化
DOI:
10.1038/srep36436
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发表时间:
2016-11-07
影响因子:
4.6
通讯作者:
Jiang HX
中科院分区:
文献类型:
--
作者:
Hu BL;Shi C;Lei RE;Lu DH;Luo W;Qin SY;Zhou Y;Jiang HX
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 fibrosisin vivoandin 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.
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影响因子:
3.3
作者:
Cui, Lei;Jia, Xin;Zhu, Huixia
通讯作者:
Zhu, Huixia
影响因子:
3.4
作者:
Ge WS;Wang YJ;Wu JX;Fan JG;Chen YW;Zhu L
通讯作者:
Zhu L
影响因子:
5.3
作者:
Zhang F;Zhang Z;Chen L;Kong D;Zhang X;Lu C;Lu Y;Zheng S
通讯作者:
Zheng S
影响因子:
13.5
作者:
Kong, Xiaoni;Feng, Dechun;Wang, Hua;Hong, Feng;Bertola, Adeline;Wang, Fu-Sheng;Gao, Bin
通讯作者:
Gao, Bin
影响因子:
--
作者:
Hassan, Zeinab Korany;Al-Olayan, Ebtisam M.
通讯作者:
Al-Olayan, Ebtisam M.