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Perturbation by lysophosphatidylcholine of membrane permeability in cultured vascular smooth muscle and endothelial cells.

Authors
  • Leung, Y M
  • Xion, Y
  • Ou, Y J
  • Kwan, C Y
Type
Published Article
Journal
Life Sciences
Publisher
Elsevier
Publication Date
Jan 01, 1998
Volume
63
Issue
11
Pages
965–973
Identifiers
PMID: 9747897
Source
Medline
License
Unknown

Abstract

Lysophosphatidylcholine (LPC), a major component of oxidized low-density lipoprotein found in atherosclerotic arterial walls, has been shown to have insignificant effect on arterial contraction but cause an impairment of endothelium-dependent relaxation (EDR). The aim of this study was to compare the degree of LPC-induced perturbation in the plasma membrane of cultured aortic smooth muscle cells (SMC) and endothelial cells (EC). In contractility studies phenylephrine (PE) elicited a sustained contraction and a subsequent addition of acetylcholine (ACh) caused an almost complete relaxation. Preincubation of endothelium-intact aortic rings with LPC did not significantly affect PE-elicited contraction but substantially inhibited ACh-triggered relaxation. Such inhibition by LPC was both concentration- and time-dependent. LPC also inhibited relaxation triggered by extracellular ATP and cyclopiazonic acid. Exposure of cultured EC to LPC (30 microM) resulted in an elevation of [Ca2+]i with a lag period of some 25 min. Following [Ca2+]i elevation, addition of Ni2+ resulted in a rapid entry of this ion into the cell. In addition, fura-2 leak-out was observed. Exposure of cultured SMC to 30 microM LPC also resulted in [Ca2+]i elevation and Ni2+ entry. However, LPC did not cause fura-2 leak-out in SMC. Also, LPC raised [Ca2+]i at a slower rate in SMC than in EC. Our results suggest that the plasma membrane of EC is more susceptible to LPC-induced derangement than that of SMC. This may contribute in part to the selective impairment of EDR by LPC.

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