AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 273: H1215-H1222, 1997;
0363-6135/97 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ota, Y.
Right arrow Articles by Yasue, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ota, Y.
Right arrow Articles by Yasue, H.

AJP - Heart and Circulatory Physiology, Vol 273, Issue 3 1215-H1222, Copyright © 1997 by American Physiological Society


ARTICLES

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

Y. Ota, K. Kugiyama, S. Sugiyama, T. Matsumura, T. Terano and H. Yasue
Division of Cardiology, Kumamoto University School of Medicine, Japan.

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.


This article has been cited by other articles:


Home page
CirculationHome page
V. Deckert, G. Lizard, N. Duverger, A. Athias, V. Palleau, F. Emmanuel, M. Moisant, P. Gambert, C. Lallemant, and L. Lagrost
Impairment of Endothelium-Dependent Arterial Relaxation By High-Fat Feeding in ApoE-Deficient Mice : Toward Normalization By Human ApoA-I Expression
Circulation, September 14, 1999; 100(11): 1230 - 1235.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
C. DESRUMAUX, V. DECKERT, A. ATHIAS, D. MASSON, G. LIZARD, V. PALLEAU, P. GAMBERT, and L. LAGROST
Plasma phospholipid transfer protein prevents vascular endothelium dysfunction by delivering {alpha}-tocopherol to endothelial cells
FASEB J, May 1, 1999; 13(8): 883 - 892.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online