Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin
| Autor: | Wei Luo, Dong-Hong Lu, Bang-li Hu, Cheng Shi, Ronge Lei, Hai-Xing Jiang, Shanyu Qin, You Zhou |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Liver Cirrhosis Male STAT3 Transcription Factor Pathology medicine.medical_specialty Beta-catenin Apoptosis Nerve Tissue Proteins Collagen Type I Article Cell Line Interleukin 22 Rats Sprague-Dawley Transforming Growth Factor beta1 03 medical and health sciences Downregulation and upregulation microRNA medicine Hepatic Stellate Cells Animals STAT3 Cell Proliferation Armadillo Domain Proteins Multidisciplinary biology Interleukins Interleukin Antagomirs R1 Actins Recombinant Proteins Rats Up-Regulation MicroRNAs 030104 developmental biology Cancer research biology.protein Hepatic stellate cell Sequence Alignment |
| Zdroj: | Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/srep36436 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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