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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
Author(s) -
Liu Huifang,
Wang Xin,
Wang ZhengYu,
Li Lingzhi
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29329
Subject(s) - gene knockdown , diabetic nephropathy , pathogenesis , cell growth , fibrosis , cancer research , fibroblast , transforming growth factor , cell , downregulation and upregulation , growth factor , chemistry , microbiology and biotechnology , endocrinology , kidney , biology , medicine , apoptosis , cell culture , receptor , gene , biochemistry , genetics
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‐FGF11 axis, and explored the underlying mechanism in regulating DN pathogenesis.