Transcriptome regulation by miR-210 in hypoxic glomerular endothelium [RNA-seq]

Hypoxia occurs in both acute and chronic kidney diseases. Despite the central role of tubular injury in acute kidney injury (AKI), a hallmark feature is a reduction in glomerular filtration rate. There is now an increasing interest in the effect of direct injury to the renal vasculature and its potential role in the pathogenesis of AKI. In this study, we profiled glomerular endothelial miRNA and mRNA changes in response to hypoxia in vitro. We identified significant induction of a hypoxia associated miRNA, miR-210-3p, which enhanced cellular glycolytic capacity. Furthermore, integrated transcriptomic analysis identified HIF1A and TFRC as putative miR-210-3p targets. This was corroborated by the strong correlation in glomerular endothelial TfR1 and HIF-1α protein expression in kidney tissue samples. Collectively, our study uncovered a compensatory mechanism in which miR-210-3p supports glomerular endothelial adaptation by modulating bioenergetics, thereby fine-tuning hypoxia responses and limiting cellular injury.