Abstract

This study aims to identify potential microRNAs (miRNAs) contribute to liver fibrosis progression and investigate how the miRNA is involved. We recruited totally 58 patients. Magnetic resonance imaging was employed to detect fibrosis. Classification of liver fibrosis was carried out by Ishak scoring system. Cell viability was tested using cell counting kit-8. Measurements of mRNA and protein expressions were conducted using real-time quantitative polymerase chain reaction and western blotting. Luciferase reporter assay was recruited for determination of miR-29b-3p targets. We found that relative enhancement (RE) values were reduced with the increases in fibrosis stages and was negatively associated with Ishak scores. In comparison with patients without liver fibrosis, miR-29b-3p level was remarkably reduced in those with liver fibrosis. Its level was found to be positively associated with RE values. Transforming growth factor beta 1 (TGF-β1)-induced hepatic stellate cell (HSC) activation significantly decreased miR-29b-3p expression. However, miR-29b-3p overexpression repressed TGF-β1-induced collagen I protein and alpha-smooth muscle actin (α-SMA) expression. As expected, its overexpression also reduced cell viability. We found that miR-29b-3p directly bind to signal transducer and activator of transcription 3 (STAT3) and suppressed its expression. Our study demonstrates that low expression of miR-29b-3p may contribute to the progression of liver fibrosis by suppressing STAT3.

中文翻译：

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肝microRNA-29b-3p与磁共振成像的相对增强值呈正相关，并抑制肝纤维化。

摘要

这项研究旨在确定潜在的微小RNA（miRNA）有助于肝纤维化的进展，并研究miRNA如何参与其中。我们共招募了58名患者。磁共振成像被用来检测纤维化。肝纤维化的分类通过Ishak评分系统进行。使用细胞计数试剂盒8测试细胞活力。使用实时定量聚合酶链反应和蛋白质印迹法进行mRNA和蛋白质表达的测量。募集了萤光素酶记者测定法来确定miR-29b-3p靶标。我们发现，相对增强（RE）值随着纤维化阶段的增加而降低，并且与Ishak得分呈负相关。与没有肝纤维化的患者相比，肝纤维化患者的miR-29b-3p水平显着降低。发现其水平与RE值正相关。转化生长因子β1（TGF-β1）诱导的肝星状细胞（HSC）激活显着降低了miR-29b-3p表达。但是，miR-29b-3p的过表达抑制了TGF-β1诱导的胶原I蛋白和α-平滑肌肌动蛋白（α-SMA）的表达。如预期的那样，其过表达也降低了细胞活力。我们发现，miR-29b-3p直接与信号转导子和转录激活子3（STAT3）结合并抑制其表达。我们的研究表明，miR-29b-3p的低表达可能通过抑制STAT3来促进肝纤维化的进展。miR-29b-3p过表达抑制TGF-β1诱导的胶原I蛋白和α平滑肌肌动蛋白（α-SMA）的表达。如预期的那样，其过表达也降低了细胞活力。我们发现，miR-29b-3p直接与信号转导子和转录激活子3（STAT3）结合并抑制其表达。我们的研究表明，miR-29b-3p的低表达可能通过抑制STAT3来促进肝纤维化的进展。miR-29b-3p过表达抑制TGF-β1诱导的胶原I蛋白和α平滑肌肌动蛋白（α-SMA）的表达。如预期的那样，其过表达也降低了细胞活力。我们发现，miR-29b-3p直接与信号转导子和转录激活子3（STAT3）结合并抑制其表达。我们的研究表明，miR-29b-3p的低表达可能通过抑制STAT3来促进肝纤维化的进展。