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Pharmacological inhibition of the F -ATPase/P2Y pathway suppresses the effect of apolipoprotein A1 on endothelial nitric oxide synthesis and vasorelaxation.

Acta Physiol (Oxf). 2019;

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PCR Cloning and Subcloning	… 4.1 - Materials. Collagenase type I from Clostridium histolyticum and M-199 medium were purchased from Gibco, Life Technologies (USA). Endothelial Cell Growth Medium-2 BulletKit (EGM-2) was purchased from Clonetics, Lonza (Walkersville, MD, USA) …	Get A Quote

摘要

The contribution of apolipoprotein A1 (APOA1)， the major apolipoprotein of high-density lipoprotein (HDL)， to endothelium-dependent vasodilatation is unclear， and there is little information regarding endothelial receptors involved in this effect. Ecto-F -ATPase is a receptor for APOA1， and its activity in endothelial cells is coupled to adenosine diphosphate (ADP)-sensitive P2Y receptors (P2Y ADP receptors). Ecto-F -ATPase is involved in APOA1-mediated cell proliferation and HDL transcytosis. Here， we investigated the effect of lipid-free APOA1 and the involvement of ecto-F -ATPase and P2Y ADP receptors on nitric oxide (NO) synthesis and the regulation of vascular tone.