Effects of circAASS overexpression in human HK2 cells

The mechanism underlying circRNA-mediated maintenance of mitochondrial function remains largely unknown. Our study found circAASS was downregulated in renal cortex from mice suffered ischemic reperfusion (IR)-induced acute kidney injury (AKI). Functional study demonstrated that circAASS regulated mitochondrial homeostasis in tubular epithelial cells (TECs). Therefore, to reveal the mechanisms underlying the anti-injury effects of circAASS in TECs. circAASS was overexpressed in hypoxia/reperfusion treated- human immortalized cell line HK2 cells. RNA sequencing was performed and the dysregulated mRNAs were found. Overall design: RNA-seq profiling of HK2 cells transfected with circAASS-overexpressing plasmids or empty vector (control plasmids) at 24 hours post hypoxia/reperfusion treatment.