ArticleIrish journal of medical science2020
Research on promoting liver fibrosis injury by the targeted regulation of miR-202 for HGF to activate HSC.
Article in Irish journal of medical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- TEAD4-mediated upregulation of LPAR3 augments hepatic stellate cell activation in portal hypertension.Cell biology and toxicology · 2025Article
- Naringenin alleviates liver fibrosis by triggering autophagy-dependent ferroptosis in hepatic stellate cells.Heliyon · 2024Article
- MiR-34a promotes fibrosis of hepatic stellate cells via the TGF-β pathway.Annals of translational medicine · 2021Article
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7 authors at 2 institutions in 1 country.
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Abstract
backgroundLiver fibrosis is the primary cause of liver cirrhosis and hepatocellular carcinoma and leads to considerable morbidity and mortality. Recent studies have shown that microRNAs are associated with fibrotic processes in liver disorders, but the exact role of miR-202 is still unclear, and its related mechanisms are not fully understood.
aimsThe aim of this research is to analyze the regarded regulation of miR-202 on HGF and its role in the pathological progress of liver fibrosis.
methodsIn the present study, qRT-PCR was used to detect the expression level of miR-202 in serum of patients with liver fibrosis and to compare its expression in patients with different pathological stages. HGF was predicted to be the target gene of miR-202 by TargetScan and was verified by Dual-luciferase reporter gene assay. qRT-PCR and western blot were used to detect the regulatory effect of mir-202 on the mRNA and protein of HGF; effect of miR-202 on the expression of fibrosis factors α-smooth muscle actin (α-SMA), FSP1, and collagen was detected; effect of miR-202 on liver fibrosis in mice was detected by establishing CCL4-induced mouse model.
resultsWe found that the expression level of miR-202 in serum of patients with liver fibrosis was significantly higher than that of healthy people, and increased with the increase of fibrosis; miR-202 inhibited the expression level of mRNA and protein of HGF by combining with the 3'-UTR of HGF; the expression level of miR-202 significantly increased after hepatic stellate cells (HSC) were stimulated by AngII; the overexpression of miR-202 could up-regulate the expression of fibrotic factors α-SMA, FSP1, and collagen I. In addition, miR-202 up-regulated the expression of collagen I and collagen III in liver tissue of mice with liver fibrosis and promoted the progress of liver fibrosis.
conclusionsmiR-202 could negatively regulate the expression of target gene HGF, activated HSC, and increased the expression levels of various fibrosis factors, and the pathological process of liver fibrosis injury was promoted.
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