MiR-29a and miR-652 Attenuate Liver Fibrosis by Inhibiting the Differentiation of CD4+ T Cells
Autor: | Ji Xuan, Wei Wen, Mei Shao, Shu-Lin Guo, Ya Yang, Hua-Bing Xu, Ang Huang |
---|---|
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
CD4-Positive T-Lymphocytes Liver Cirrhosis Male Physiology Aspartate transaminase CCL4 Flow cytometry 03 medical and health sciences Mice Western blot Fibrosis In vivo medicine Animals Molecular Biology Carbon Tetrachloride Cells Cultured medicine.diagnostic_test biology business.industry Cell Differentiation Cell Biology General Medicine medicine.disease Mice Inbred C57BL MicroRNAs 030104 developmental biology Alanine transaminase Cancer research biology.protein Liver function business |
Zdroj: | Cell structure and function. 42(2) |
ISSN: | 1347-3700 |
Popis: | Background Liver fibrosis is the response of liver diseases that puzzles patients. MiRNAs were involved in the regulating processes of liver fibrosis. This study aims to investigate the effects of ARRB1 mediated by miR-29a and miR-652 on liver fibrosis and its possible mechanism. Methods Liver fibrosis of mice was induced by intraperitoneal injection of CCl4. Liver function was observed by the levels of alanine transaminase (ALT) and aspartate transaminase (AST). Flow cytometry was used to detect the percent of T helper17 (Th17). ELISA (Enzyme linked immunoassay) was used to detect the levels of Interleukin-17 (IL-17) and Interleukin-22 (IL-22). Real-time PCR was used to detect the expression of IL-17A, IL-22, miR-29a, miR-652 and β-Arrestin 1 Gene (ARRB1). Western blot was used to detect the protein expression of ARRB1. Results CCl4 supplementation significantly increased the level of ALT and AST, the percent of Th17, the level of IL-17A, IL-22, miR-29a and miR-652, but decreased ARRB1. Overexpression of miR-29a/miR-652 prominently decreased Th17, IL-17A, IL-22 and ARRB1 in the normal CD4+ T cells. Both miR-29a and miR-652 targeted ARRB1 to regulate its expression. The effects of miR-29a/miR-652 overexpression on CD4+ T cells were reversed by ARRB1 overexpression. In vivo experiments demonstrated the protective role of miR-29a/miR-652 overexpression on liver fibrosis. Conclusion ARRB1 mediated by miR-29a and miR-652 probably involved in the CD4+ T cells differentiation in patients with liver fibrosis, and functioned as a biomarker of fibrosis liver.Key words: liver fibrosis, miR-29a, miR-652, ARRB1, CD4+ T cells. |
Databáze: | OpenAIRE |
Externí odkaz: |