作者: Le Tao , Liu Wu , Wei Zhang , Wen-ting Ma , Guang-yue Yang
DOI: 10.1016/J.LFS.2020.117572
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摘要: Abstract Aims Liver fibrosis is a chronic liver disease characterized by hepatic stellate cell (HSC) activation. Peroxisome proliferator-activated receptor gamma (PPARγ) play an important role in HSC This study aimed to investigate the of PPARγ progression human and mechanism which microRNA-942 regulates Methods 70 hepatitis B (CHB) patients tissues were used assess PPARγ, α-SMA miR-942 levels immunoblot real-time PCR. Human primary HSCs or LX2 cells perform multiple molecular experiments based on transfection small interfering RNA (siRNA) co-transfection microRNA inhibitor. Site-directed mutagenesis luciferase reporter assays identify targets. expression localization co-localization between determined fluorescence situ hybridization (FISH). Key findings The mRNA was decreased activated CHB with fibrosis, negatively correlated F stage α-SMA. via targeting 3′UTR. Inhibiting promoted TGFβ1 induced activation, this effect blocked after inhibiting miR-942. Moreover, mainly expressed fibrous septa fibrosis. Significance decreasing activation Hence, regulating may be promising therapeutic strategy for