Endothelium

LAV-BPIFB4 isoform modulates eNOS signaling through Ca2+/PKC-alpha dependent mechanism

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.

Establishment and long-term culture of human cystic fibrosis endothelial cells

Endothelial cell (EC) dysfunction has been reported in cystic fibrosis (CF) patients. Thus, the availability of CF EC is
paramount to uncover mechanisms of endothelial dysfunction in CF. Using collagenase digestion, we isolated cells from
small fragments of pulmonary artery dissected from non-CF lobes or explanted CF lungs. These cells were a
heterogeneous mixture, containing variable percentages of EC. To obtain virtually pure pulmonary artery endothelial cells

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