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

Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin.
复制标题

Interleukin-22 通过 miR-200a/β-catenin 改善肝纤维化

DOI:
10.1038/srep36436
复制
发表时间:
2016-11-07
期刊:
影响因子:
4.6
通讯作者:
Jiang HX
Jiang HX
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Hu BL;Shi C;Lei RE;Lu DH;Luo W;Qin SY;Zhou Y;Jiang HX

文献摘要

参考文献

被引文献

相似文献

IL-22通过抑制肝星状细胞(HSC)来改善肝纤维化,并且miR-200 a的缺失与肝纤维化的发展相关。本研究旨在探讨IL-22和miR-200 a在体内和体外调节肝纤维化中的相互作用。我们观察到IL-22显著降低HSC的增殖并增加p-STAT 3的表达。荧光素酶报告基因检测证实β-catenin是miR-200 a的靶基因,上调miR-200 a可显著抑制HSC增殖,降低β-catenin的表达。IL-22处理增加HSC中miR-200 a的表达并降低HSC中β-catenin的表达。IL-22处理后,肝纤维化大鼠肝脏中p-STAT 3和miR-200 a的表达升高,而β-catenin的表达降低。β-catenin和p-STAT 3在肝纤维化大鼠肝脏和HSC中的表达水平呈负相关。β-catenin上调可抑制HSC中p-STAT 3的表达。结论IL-22可能通过上调miR-200 a的表达,下调β-catenin的表达,抑制HSC活化,减轻肝纤维化,提示IL-22/STAT 3和β-catenin通路之间可能存在交叉作用。
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.
DOI: 10.1111/jphp.12283
发表时间: 2014-11-01
影响因子: 3.3
作者:
Cui, Lei;Jia, Xin;Zhu, Huixia
通讯作者: Zhu, Huixia
DOI: 10.3892/mmr.2014.2099
发表时间: 2014-06
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
姜黄素可减弱肝纤维化中的血管生成并抑制肝星状细胞的血管生成特性
DOI: 10.1111/jcmm.12286
发表时间: 2014-07
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
DOI: 10.1002/hep.25744
发表时间: 2012-09
期刊: HEPATOLOGY
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
DOI: 10.7314/apjcp.2012.13.11.5405
发表时间: 2012-01-01
影响因子: --
作者:
Hassan, Zeinab Korany;Al-Olayan, Ebtisam M.
通讯作者: Al-Olayan, Ebtisam M.