LAV-BPIFB4 isoform modulates eNOS signaling through Ca2+/PKC-alpha dependent mechanism
01 Pubblicazione su rivista
Spinelli Chiara Carmela, Carrizzo Albino, Ferrario Anna, Villa Francesco, Damato Antonio, Ambrosio Mariateresa, Madonna Michele, Frati Giacomo, Fucile Sergio, Sciaccaluga Miriam, Capunzo Mario, Calì Gaetano, Milanesi Luciano, Maciag Anna, Puca Annibale Alessandro, Vecchione Carmine
DOI: 10.1093/cvr/cvx072
ISSN: 0008-6363
Aging is associated with impairment of endothelial nitric oxide synthase (eNOS) and progressive reduction in endothelial function. A genetic study on long-living individuals - who are characterized by delays in aging and in the onset of cardiovascular disease - previously revealed I229V ( rs2070325 ) in BPIFB4 as a longevity-associated variant (LAV); the LAV protein enhanced endothelial NO production and vasorelaxation through a PERK/14-3-3/HSP90 signal. Here, we further characterize the molecular mechanisms underlying LAV-BPIFB4-dependent enhancement of vascular function.