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Schisandrin B attenuates renal fibrosis via miR-30e-mediated inhibition of EMT.
Toxicology and Applied Pharmacology ( IF 3.3 ) Pub Date : 2019-11-05 , DOI: 10.1016/j.taap.2019.114769 Guangxu Cao 1 , Shuang Li 2 , Hezhan Shi 1 , Peidi Yin 1 , Jialing Chen 1 , Huifeng Li 1 , Ying Zhong 1 , Li-Ting Diao 3 , Bin Du 1
Toxicology and Applied Pharmacology ( IF 3.3 ) Pub Date : 2019-11-05 , DOI: 10.1016/j.taap.2019.114769 Guangxu Cao 1 , Shuang Li 2 , Hezhan Shi 1 , Peidi Yin 1 , Jialing Chen 1 , Huifeng Li 1 , Ying Zhong 1 , Li-Ting Diao 3 , Bin Du 1
Affiliation
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Tubulointerstitial fibrosis (TIF) is the main pathologic feature of end-stage renal disease. Epithelial-mesenchymal transition (EMT) of proximal tubular cells (PTCs) is one of the most significant features of TIF. MicroRNAs play critical roles during EMT in TIF. However, whether miRNAs can be used as therapeutic targets in TIF therapy remains undetermined. We found that miR-30e, a member of the miR-30 family, is deregulated in TGF-β1-induced PTCs, TIF mice and human fibrotic kidney tissues. Moreover, transcription factors that induce EMT, such as snail, slug, and Zeb2, were direct targets of miR-30e. Using a cell-based miR-30e promoter luciferase reporter system, Schisandrin B (Sch B) was selected for the enhancement of miR-30e transcriptional activity. Our results indicate that Sch B can decrease the expression of snail, slug, and Zeb2, thereby attenuating the EMT of PTCs during TIF by upregulating miR-30e, both in vivo and in vitro. This study shows that miR-30e can serve as a therapeutic target in the treatment of patients with TIF and that Sch B may potentially be used in therapy against renal fibrosis.
中文翻译：
五味子素B通过miR-30e介导的EMT抑制作用减轻肾纤维化。
肾小管间质纤维化（TIF）是终末期肾脏疾病的主要病理特征。近端肾小管细胞（PTC）的上皮-间质转化（EMT）是TIF的最重要特征之一。MicroRNA在TIF的EMT期间起着至关重要的作用。但是，是否可以将miRNA用作TIF治疗的靶标尚不确定。我们发现，miR-30e是miR-30家族的成员，在TGF-β1诱导的PTC，TIF小鼠和人纤维化肾组织中被失调。此外，诱导EMT的转录因子，例如蜗牛，和Zeb2，是miR-30e的直接靶标。使用基于细胞的miR-30e启动子荧光素酶报告系统，选择五味子素B（Sch B）来增强miR-30e转录活性。我们的结果表明，Sch B可以降低蜗牛，nail和Zeb2的表达，从而通过在体内和体外上调miR-30e来减弱TIF期间PTC的EMT。这项研究表明，miR-30e可以作为TIF患者的治疗靶标，Sch B可能潜在地用于抗肾纤维化的治疗。
更新日期：2019-11-06
中文翻译：
五味子素B通过miR-30e介导的EMT抑制作用减轻肾纤维化。
肾小管间质纤维化（TIF）是终末期肾脏疾病的主要病理特征。近端肾小管细胞（PTC）的上皮-间质转化（EMT）是TIF的最重要特征之一。MicroRNA在TIF的EMT期间起着至关重要的作用。但是，是否可以将miRNA用作TIF治疗的靶标尚不确定。我们发现，miR-30e是miR-30家族的成员，在TGF-β1诱导的PTC，TIF小鼠和人纤维化肾组织中被失调。此外，诱导EMT的转录因子，例如蜗牛，和Zeb2，是miR-30e的直接靶标。使用基于细胞的miR-30e启动子荧光素酶报告系统，选择五味子素B（Sch B）来增强miR-30e转录活性。我们的结果表明，Sch B可以降低蜗牛，nail和Zeb2的表达，从而通过在体内和体外上调miR-30e来减弱TIF期间PTC的EMT。这项研究表明，miR-30e可以作为TIF患者的治疗靶标，Sch B可能潜在地用于抗肾纤维化的治疗。
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