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Background  Damage to the renal microvasculature is a hallmark of renal ischemia-reperfusion injury (IRI)–mediated AKI. The  miR-17∼92  miRNA cluster (encoding  miR-17 ,  -18a ,  -19a ,  -20a ,  -19b-1 , and  -92a-1 ) regulates angiogenesis in multiple settings, but no definitive role in renal endothelium during AKI pathogenesis has been established.    Methods  Antibodies bound to magnetic beads were utilized to selectively enrich for renal endothelial cells from mice. Endothelial-specific  miR-17∼92  knockout ( miR-17∼92   endo−/−  ) mice were generated and given renal IRI. Mice were monitored for the development of AKI using serum chemistries and histology and for renal blood flow using magnetic resonance imaging (MRI) and laser Doppler imaging. Mice were treated with miRNA mimics during renal IRI, and therapeutic efficacies were evaluated.    Results   miR-17 ,  -18a ,  -20a ,  -19b , and  pri–miR-17∼92  are dynamically regulated in renal endothelial cells after renal IRI.  miR-17∼92   endo−/−   exacerbates renal IRI in male and female mice. Specifically,  miR-17∼92   endo−/−   promotes renal tubular injury, reduces renal blood flow, promotes microvascular rarefaction, increases renal oxidative stress, and promotes macrophage infiltration to injured kidneys. The potent antiangiogenic factor thrombospondin 1 (TSP1) is highly expressed in renal endothelium in  miR-17∼92   endo−/−   after renal IRI and is a target of  miR-18a  and  miR-19a/b .  miR-17∼92  is critical in the angiogenic response after renal IRI, which treatment with  miR-18a  and  miR-19b  mimics can mitigate.    Conclusions  These data suggest that endothelial-derived  miR-17∼92  stimulates a reparative response in damaged renal vasculature during renal IRI by regulating angiogenic pathways.

Endothelial-Derived miR-17∼92 Promotes Angiogenesis to Protect against Renal Ischemia-Reperfusion Injury