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- Title
miRNA-338-3p/CDK4 signaling pathway suppressed hepatic stellate cell activation and proliferation.
- Authors
Bensong Duan; Jiangfeng Hu; Tongyangzi Zhang; Xu Luo; Yi Zhou; Shun Liu; Liang Zhu; Cheng Wu; Wenxiang Liu; Chao Chen; Hengjun Gao; Duan, Bensong; Hu, Jiangfeng; Zhang, Tongyangzi; Luo, Xu; Zhou, Yi; Liu, Shun; Zhu, Liang; Wu, Cheng; Liu, Wenxiang
- Abstract
<bold>Background: </bold>Activated hepatic stellate cell (HSC) is the main fibrogenic cell type in the injured liver. miRNA plays an important role in activation and proliferation of HSC.<bold>Methods: </bold>Our previous study examined the expression profiles of microRNAs in quiescent and activated HSC. Real-time PCR and western blot were used to detect the expression of Collagen type I (Col 1) and Alpha-Smooth Muscle Actin (α-SMA). CCK-8 and Edu assay was used to measure the proliferation rate of HSC. Luciferase reporter gene assay was used to tested the binding between miR-338-3p and Cyclin-dependent kinase 4 (CDK4).<bold>Results: </bold>We found overexpression of miR-338-3p could inhibit Col 1 and α-SMA, two major HSC activation markers, whereas miR-338-3p inhibitor could promote them. Besides, miR-338-3p overexpression could suppress the growth rate of HSC. Further, we found that CDK4, a pleiotropic signaling protein, was a direct target gene of miR-338-3p. Moreover, we found that overexpression of CDK4 could block the effects of miR-338-3p.<bold>Conclusions: </bold>We found miR-338-3p is an anti-fibrotic miRNA which inhibits cell activation and proliferation. Our findings suggest that miR-338-3p/CDK4 signaling pathway participates in the regulation of HSC activation and growth and may act as a novel target for further anti-fibrotic therapy.
- Subjects
CYCLIN-dependent kinases; LIVER cells; MICRORNA; COLLAGEN; LUCIFERASES; CELL metabolism; RNA metabolism; MUSCLE protein metabolism; ANIMAL experimentation; CELL physiology; CELLULAR signal transduction; CIRRHOSIS of the liver; RATS; TRANSFERASES; METABOLISM
- Publication
BMC Gastroenterology, 2017, Vol 17, p1
- ISSN
1471-230X
- Publication type
journal article
- DOI
10.1186/s12876-017-0571-3