ArticleKidney diseases (Basel, Switzerland)
Enhanced miR-214 in Vascular Endothelial Cells Retards Renal Inflammation and Glomerular Sclerosis in Five-Sixths Nephrectomy Mice.
Article in Kidney diseases (Basel, Switzerland). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Vascular endothelial injury is a critical driver of renal dysfunction and glomerulosclerosis in chronic kidney disease (CKD). While endothelial damage-induced inflammation contributes to sclerosis, the underlying mechanisms remain unclear. Although miR-214 has been implicated in renal fibrosis, its role in vascular endothelial cells during glomerulosclerosis is undefined. Methods: In this study, we investigated miR-214 expression and function in renal endothelial cells using five-sixths nephrectomy (5/6Nx) mice, endothelial-specific and smooth muscle-specific miR-214 knockout models, CD31-enriched primary renal endothelial cells, and mouse aortic endothelial cells. Transcriptome analysis, bioinformatic prediction, luciferase reporter assays, cytokine profiling, and pro-inflammatory stimulation experiments were performed to evaluate the regulatory relationship between miR-214 and RELA-associated inflammatory signaling. Results: We observed significant miR-214 upregulation in renal endothelial cells of 5/6Nx mice. Endothelial-specific knockout of miR-214 aggravated glomerulosclerosis and endothelial dysfunction, whereas smooth muscle-specific knockout showed no significant effect. Transcriptome analysis revealed that miR-214 inhibition altered the NF-κB pathway, specifically upregulating RELA. Bioinformatic prediction and luciferase reporter assays supported a direct interaction between miR-214 and the RELA 3'-UTR in vitro. In CD31-enriched primary renal endothelial cells, modulation of miR-214 levels inversely regulated RELA expression. Cytokine profiling showed that miR-214 suppression enhanced pro-inflammatory secretion. Furthermore, pro-inflammatory stimulation experiments demonstrated that inhibition of miR-214 amplified RELA-associated endothelial inflammatory activation, while miR-214 overexpression attenuated it. Conclusion: Collectively, these results suggest that endothelial miR-214 protects against glomerulosclerosis by restraining RELA-associated inflammatory signaling, highlighting endothelial-targeted modulation of miR-214 as a potential therapeutic strategy for CKD-related glomerular injury.
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