Ji Xuan1,2, Shu-Lin Guo3, Ang Huang4, Hua-Bing Xu1, Mei Shao1, Ya Yang1, Wei Wen1. 1. Bayi Hospital Affiliated Nanjing University of Chinese Medicine. 2. Nanjing University of Chinese Medicine. 3. 107 Hospital of PLA. 4. Center of Non-infectious Liver Diseases, Beijing 302 Hospital.
Abstract
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.
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.
Entities:
Keywords:
ARRB1; CD4+ T cells; liver fibrosis; miR-29a; miR-652