Evaluation of renal mononuclears cells in acute kidney injury after inhibiting retinoic acid signaling in proximal tubular epithelial cells
Retinoic acid (RA) signaling is activted in proximal tubular epithelial cells (PTECs) after acute kidney injury (AKI). In these studies we evaluated the functional role of this by inducing ischemia reperfusion-induced AKI (IRI-AKI) in mice after inhibiting RA signaling in PTECs genetically. Here we evaluated the effects of this on the activation of renal mononuclear cells (MNCs) by evaluating RNA expression in CD11B+ cells isolated from kidneys after IRI-AKI. Compared with control mice, there was a reducion in expression of inflammatory marker gene expression 3 days after IRI-AKI in mice with inhibition of RAR signaling in PTECs. These findings suggest a mechanism by which inhibition of RAR signaling in PTECs is protective against AKI. Overall design: PTEC DN-RAR mice (PEPCK CRE+; Rosa26-LSL-RARaT403X), and CRE- controls (PEPCK CRE-; Rosa26-LSL-RARaT403X) underwent bilateral IRI-AKI, and bulk RNA seq performed on renal CD11B+ cells isolated using CD11B antibody coated magnetic beads 3 days after injury.