Complexes of apoA-1 with phosphatidylcholine suppress dysregulation of arterial tone by oxidized LDL

• Published in: The American journal of physiology Vol. 273; no. 3 Pt 2; p. H1215
• Main Authors: Ota, Y, Kugiyama, K, Sugiyama, S, Matsumura, T, Terano, T, Yasue, H
• Format: Journal Article
• Language: English
• Published: United States 01.09.1997
• Subjects: Analysis of Variance; Animals; Apolipoprotein A-I - pharmacology; Cells, Cultured; Coronary Vessels - drug effects; Coronary Vessels - physiology; Dimyristoylphosphatidylcholine - pharmacology; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Humans; In Vitro Techniques; Lipoproteins, LDL - antagonists & inhibitors; Lipoproteins, LDL - pharmacology; Muscle Contraction - drug effects; Muscle Contraction - physiology; Muscle Relaxation - drug effects; Muscle Tonus - drug effects; Muscle Tonus - physiology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; Swine; Thrombin - pharmacology
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajpheart.1997.273.3.h1215

The aim of this study was to determine whether apolipoprotein A-1 (apoA-1) may suppress the vasomotor dysregulation by oxidized low-density lipoprotein (ox-LDL), which is known to be an atherogenic lipoprotein. The isolated porcine coronary arterial rings and the cultured endothelial cells from the porcine coronary arteries were exposed to ox-LDL in the presence or absence of complexes of apoA-1 with dimyristoylphosphatidylcholine (DMPC/apoA-1), apoA-1 alone, or DMPC alone. DMPC/apoA-1 but not apoA-1 alone or DMPC alone was found to suppress both impairment of endothelium-dependent arterial relaxation and vasocontraction caused by ox-LDL in the isolated porcine coronary arterial rings suspended in organ chambers. DMPC/apoA-1 absorbed lysophosphatidylcholine (LPC) from ox-LDL and decreased the transfer of LPC from ox-LDL to the surface membrane of the cultured endothelial cells, but apoA-1 alone and DMPC alone had no effect. High-density lipoprotein exerted the protective actions mimicking those observed in DMPC/apoA-1. Thus DMPC/apoA-1 decreased the transfer of LPC from ox-LDL to surface membrane by absorbing LPC, leading to the suppression of ox-LDL-induced dysregulation of endothelium-dependent arterial tone. Therefore, apoA-1 appears to require formation of the complexes with phospholipids to prevent the endothelial dysfunction caused by ox-LDL.