Regulation of eNOS in Caveolae

摘要: Caveolae are a specialized subset of lipid domains that prevalent on the plasma membrane endothelial cells. They compartmentalize signal transduction molecules which regulate multiple functions including production nitric oxide (NO) by caveolae resident enzyme NO synthase (eNOS). eNOS is one three isoforms NOS generates upon conversion L-arginine to L-citrulline and it regulated mechanisms. Caveolin negatively impact activity through direct interaction with enzyme. Circulating factors known modify cardiovascular disease risk also influence In particular, high density lipoprotein cholesterol (HDL) maintains environment in caveolae, thereby promoting retention function domain causes activation via scavenger receptor class B, Type I (SR-BI)-induced kinase signaling. Estrogen binding estrogen receptors (ER) activates this occurs G protein coupling activation. Discrete within SR-BI ER mediating initiation have been identified. Counteracting promodulatory actions HDL estrogen, C-reactive (CRP) antagonizes FcγRIIB, sole inhibitory for IgG. Through their eNOS, CRP cell growth migration. Thus, signaling events invoked circulating major phenotypes importance health disease.