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首页> 外文期刊>Journal of cellular physiology. >Circ_0080425 inhibits cell proliferation and fibrosis in diabetic nephropathy via sponging miR-24-3p and targeting fibroblast growth factor 11
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Circ_0080425 inhibits cell proliferation and fibrosis in diabetic nephropathy via sponging miR-24-3p and targeting fibroblast growth factor 11

机译：Circ_0080425抑制细胞增殖通过骗取纤维化在糖尿病肾病miR-24-3p和定位纤维母细胞生长因子11

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摘要

Diabetic nephropathy (DN) is a severe end-stage kidney disease developed from diabetes mellitus. The involvement of circular RNAs (circRNAs) in modulating DN pathogenesis has been implied, but underlying mechanism is still lacking. In this study, we demonstrated that the expression of circ_0080425 correlated with the DN progression, and exerted positive effect on cell proliferation and fibrosis in mesangial cells. Further assessment suggested that circ_0080425 function as sponge harboring miR-24-3p. Moreover, miR-24-3p negatively correlated with the DN progression, and showed an antagonistic effect to circ_0080425on regulating MCs cell proliferation and fibrosis. Bioinformatics analysis predicted fibroblast growth factor 11 (FGF11) acting as direct downstream target of miR-24-3p. Indeed, the expression of FGF11 was significantly activated by circ_0080425 while suppressed by miR-24-3p. Knockdown of FGF11 resulted in a significant reduced cell proliferation rate and fibrosis. In addition, miR-24-3p inhibitor rescued the suppression of si-circ_0080425 on FGF11, suggesting that circ_0080425 competitive binding to miR-24-3p could release FGF11 from miR-24-3p suppression, which subsequently promoted DN progression.In conclusion, we have reported a novel circ_0080425-miR-24-3p-FGFll axis, and explored the underlying mechanism in regulating DN pathogenesis.
机译：糖尿病肾病(DN)是一种严重的晚期从糖尿病肾病发展。圆形rna (circRNAs)的参与调制DN发病机理一直暗示,但是潜在的机制仍然缺乏。研究中,我们证明的表达circ_0080425与DN发展,对细胞增殖并产生积极的影响在系膜细胞和纤维化。评估建议circ_0080425函数海绵窝藏miR-24-3p。与DN miR-24-3p负相关进展,显示一个对立的效果circ_0080425on调节MCs细胞增殖和纤维化。纤维母细胞生长因子11 (FGF11)担任直接下游miR-24-3p的目标。FGF11明显的表达激活circ_0080425而压抑miR-24-3p。细胞增殖率和显著减少纤维化救了si-circ_0080425的抑制FGF11,表明circ_0080425竞争力绑定miR-24-3p可以免除FGF11随后miR-24-3p抑制促进DN发展。报道一种新型circ_0080425-miR-24-3p-FGFll轴,探索底层机制调节DN发病机理。

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