Transcriptomic analysis of kidney cortex following knockdown of endothelial Klf4 on wild-type and Nos3 deficient backgrounds.
The goal of this study was to identify transcriptomic changes, mediated by the loss of endothleial Klf4, seen in glomerular microangiopathy in kidney endothelial cells. We recently reported that the endothelial-specific knockout of Krüppel-like factor 4 (Klf4) increases the susceptibility to GEnC injury and subsequent development of subacute thrombotic microangiopathy. However, the mechanism(s) mediating GEnC response to injury in thrombotic microangiopathy are poorly understood. Single nucleus RNA sequencing demonstrated an enrichment in pathways involved in angiogenesis, permeability, focal adhesion and cytoskeletal organization, specifically in the endothelial cluster in mice with endothelial loss of Klf4. Overall design: Mouse renal cortex from four distinct genotypes were analyzed with one replicate per genotype.