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MiR-1297 attenuates high glucose-induced injury in HK-2 cells via targeting COL1A2
Shujuan Wang1, Kun Sun2, Honglei Hu1
1Department of Endocrinology, Zibo Central Hospital, Zibo, China.
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.
Insights
MicroRNA-1297 (miR-1297) protects against diabetic nephropathy (DN) by downregulating COL1A2, reducing inflammation, and promoting cell survival. This suggests miR-1297 as a potential therapeutic target for DN.
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- Diabetic nephropathy (DN) is a significant complication of diabetes.
- Understanding the molecular mechanisms underlying DN progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the roles of COL1A2 and microRNA-1297 (miR-1297) in diabetic nephropathy (DN) progression.
- To elucidate the underlying molecular mechanisms involving miR-1297 and COL1A2 in vitro.
Main Methods:
- Utilized high glucose (HG)-stimulated HK-2 cells to model DN.
- Analyzed RNA and non-coding RNA profiles from the Gene Expression Omnibus (GEO) database.
- Employed dual-luciferase reporter assays, Gene Set Enrichment Analysis (GSEA), cell counting kit-8, and apoptosis assays to assess molecular interactions and cellular functions.
Main Results:
- COL1A2 was upregulated, while miR-1297 was downregulated in DN tissues and HG-treated HK-2 cells.
- miR-1297 overexpression promoted cell proliferation and inhibited apoptosis, protecting against HG-induced damage.
- miR-1297 targeted COL1A2, suppressing inflammatory pathways by reducing NFκB phosphorylation and pro-inflammatory gene expression (CCL5, ICAM1, VCAM1).
Conclusions:
- miR-1297 plays a protective role in DN by targeting COL1A2 and inhibiting inflammation.
- The miR-1297/COL1A2 axis represents a novel therapeutic strategy for DN progression.
