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MiR ‐1297 attenuates high glucose‐induced injury in HK ‐2 cells via targeting COL1A2
Author(s) -
Wang Shujuan,
Sun Kun,
Hu Honglei,
Jin Xingqian,
Wang Zhenzhen,
Zhang Hongmei,
Zhao Xiaodong
Publication year - 2021
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.13881
Subject(s) - gene knockdown , transfection , apoptosis , microbiology and biotechnology , microrna , reporter gene , gene expression , biology , gene , genetics
Background In this study, we aimed to explore whether COL1A2 and miR‐1297 participated in the progression of diabetic nephropathy (DN) in vitro and classified the underlying mechanisms. Methods d ‐Glucose (30 mM; high glucose, HG)‐stimulated HK‐2 cells were used to mimic DN condition. RNA and non‐coding RNA profiles were from Gene Expression Omnibus (GEO) database. The interaction between miR‐1297 and COL1A2 was measured by dual‐luciferase reporter assay. Gene Set Enrichment Analysis (GSEA) method was conducted to analyse COL1A2‐associated signalling pathways. The role of miR‐1297/COL1A2 in biological behaviours of HG‐induced HK‐2 cells were analysed by cell counting kit‐8 and apoptosis assays. Results Bioinformatics analysis revealed that COL1A2 was up‐regulated in DN tissues. We predicted and verified miR‐1297 as the regulatory miRNA of COL1A2, and the expression of miR‐1297 was decreased in DN tissues and HG‐stimulated HK‐2 cells. Overexpression of miR‐1297 could promote cell proliferation and inhibit apoptosis to protect HK‐2 cells from HG‐induced damage. And knockdown of COL1A2 enhanced the protective effects of miR‐1297 on HG‐stimulated HK‐2 cells. GSEA results revealed that several inflammatory pathways were enriched in COL1A2 high‐expression group. Meanwhile, transfection of miR‐1297 reduced the phosphorylation of NFκB and expression of three important pro‐inflammatory genes including cytokine CCL5, adhesion molecules ICAM1 and VCAM1 via targeting COL1A2. These results suggested that miR‐1297 protected HG‐treated HK‐2 cells probably through suppressing inflammation via targeting COL1A2. Conclusion This study sheds a light on the role miR‐1297/COL1A2 in DN progression and provides a novel promising therapy strategy for suppressing DN progression.