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Published:
Jun 4, 2022DOI:
10.4314/tjpr.v21i4.8Keywords:
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Main Article Content
Effects of microRNA-129-5p on hepatic fibrosis and primary hepatic stellate cell proliferation and migration in rats
Abstract
Purpose: To investigate the effects and mechanism of microRNA (miR)-129-5p in hepatic fibrosis and hepatic stellate cell proliferation and migration in rats.
Methods: Forty Sprague-Dawley rats were randomly divided into control and model groups. Carbon tetrachloride (CCl4)-induced hepatic fibrosis was established in the model group. Hematoxylin and eosin staining was used to observe rat liver pathological sections. Sirius red staining was used to assess collagen deposition, while quantitative real-time polymerase chain reaction was used to evaluate miR- 129-5p expression in the rat liver during hepatic fibrosis. Three groups of rat primary hepatic stellate cells (HSCs) (miR-129-5p overexpression group, negative control lentivirus group and blank control group) were prepared. Cell proliferation and migration were determined using Cell Counting Kit-8 and Transwell assay, respectively. Serum- and glucocorticoid-regulated kinase 3 (SGK3), β-catenin, and α-smooth muscle actin (α-SMA) expression were evaluated by Western blotting, while dual luciferase
reporter gene assay was used to evaluate whether SGK3 is an miR-129-5p target.
Results: miR-129-5p expression was significantly reduced during the progression of CCl4-induced rat hepatic fibrosis (p < 0.05). The proliferation rate and migration ability of the primary HSCs in the miR- 129-5p mimics group were significantly lower than those in the miR-129-5p NC and blank control groups (p < 0.05). Protein expression of SGK3, β-catenin, and α-SMA in the miR-129-5p mimics group was reduced (p < 0.05), and miR-129-5p showed targeted binding to SGK3.
Conclusion: MiR-129-5p down-regulates the expression of β-catenin through targeted regulation of SGK3 to inhibit HSC activation, providing novel insight into design of a potential treatment strategy for hepatic fibrosis.
