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微小RNA-26-5p通过调控PTEN/PI3K/AKT信号通路抑制环孢素A诱导的牙龈成纤维细胞过度生长。

miRNA-26-5p inhibits cyclosporine A-induced overgrowth of gingival fibroblasts by regulating PTEN/PI3K/AKT pathway.

作者信息

Hu Qiyong, Guo Nadan, Zhao Yuting, Chen Yi, Zhang Peng, Shen Wei, Gu Ziya

机构信息

Hangzhou West Dental Hospital, Hangzhou, China.

Hangzhou Dental Hospital, Huzhou Branch, Huzhou, China.

出版信息

Growth Factors. 2020 Dec;38(5-6):291-301. doi: 10.1080/08977194.2021.1967343. Epub 2021 Aug 24.

Abstract

We evaluated the effect of cyclosporine A (CsA) administration on the level of miR-26-5p in rat gingival tissues and human gingival fibroblasts (HGFs) by qRT-PCR assay. Further, we conducted Western blotting and immunohistochemical analysis to assess the expressions of PTEN, PI3K, and p-AKT, and evaluated cell proliferation of HGFs by MTT assay. CsA treatment significantly downregulated the expressions of miR-26-5p and PTEN and upregulated the expressions of PI3K and p-AKT in both rat gingival tissues and HGFs. Overexpression of miR-26-5p inhibited CsA-induced overgrowth of HGFs, whereas knockdown of miR-26-5p promoted the overgrowth. PTEN knockdown not only promoted CsA-induced overgrowth of human HGFs but also reversed the repressive effects of miR-26-5p on CsA-induced overgrowth of HGFs. Our results revealed that miRNA-26-5p could repress CsA-induced overgrowth of human HGFs by regulating PTEN/PI3K/AKT pathway.

摘要

我们通过qRT-PCR检测评估了环孢素A(CsA)给药对大鼠牙龈组织和人牙龈成纤维细胞(HGFs)中miR-26-5p水平的影响。此外,我们进行了蛋白质免疫印迹和免疫组织化学分析以评估PTEN、PI3K和p-AKT的表达,并通过MTT检测评估HGFs的细胞增殖。CsA处理显著下调了大鼠牙龈组织和HGFs中miR-26-5p和PTEN的表达,并上调了PI3K和p-AKT的表达。miR-26-5p的过表达抑制了CsA诱导的HGFs过度生长,而miR-26-5p的敲低则促进了过度生长。PTEN的敲低不仅促进了CsA诱导的人HGFs过度生长,还逆转了miR-26-5p对CsA诱导的HGFs过度生长的抑制作用。我们的结果表明,miRNA-26-5p可通过调节PTEN/PI3K/AKT途径抑制CsA诱导的人HGFs过度生长。

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