Retinoic Acid Signaling Coordinates Macrophage-Dependent Injury and Repair after AKI.

ABSTRACT: Retinoic acid (RA) has been used therapeutically to reduce injury and fibrosis in models of AKI, but little is known about the regulation of this pathway and what role it has in regulating injury and repair after AKI. In these studies, we show that RA signaling is activated in mouse and zebrafish models of AKI, and that these responses limit the extent of injury and promote normal repair. These effects were mediated through a novel mechanism by which RA signaling coordinated the dynamic equilibrium of inflammatory M1 spectrum versus alternatively activated M2 spectrum macrophages. Our data suggest that locally synthesized RA represses proinflammatory macrophages, thereby reducing macrophage-dependent injury post-AKI, and activates RA signaling in injured tubular epithelium, which in turn p

SUBMITTER: Chiba T 

PROVIDER: S-EPMC4731115 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature