Opposing Effects on Vascular Smooth Muscle Cell Proliferation and Macrophage-induced Inflammation Reveal a Protective Role for the Proresolving Lipid Mediator Receptor ChemR23 in Intimal Hyperplasia.

ABSTRACT: Intimal hyperplasia remains a significant clinical problem in for example coronary artery bypass graft failure. Since omega-3 fatty acids reduce intimal hyperplasia, we hypothesized that the G protein-coupled receptor ChemR23 for the omega-3-derived pro-resolving lipid mediator resolvin E1 drives those effects. ChemR23^+/+ and ChemR23^-/- mice were generated with or without introduction of the Caenorhabditis elegans fat-1 transgene, which leads to an endogenous omega-3 fatty acid synthesis and thus increasing the substrate for resolvin E1 formation. ChemR23 deletion significantly increased intimal hyperplasia 28 days after ligation of the left common carotid artery. Mice expressing the fat-1 transgene showed reduced intimal hyperplasia independently

SUBMITTER: Artiach G 

PROVIDER: S-EPMC6255922 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature