NDLI: Oxidized phospholipid species promote in vivo differential cx43 phosphorylation and vascular smooth muscle cell proliferation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Johnstone, Scott R. Ross, Jeremy Rizzo, Michael J. Straub, Adam C. Lampe, Paul D. Leitinger, Norbert Isakson, Brant E.
Description	Country affiliation: United States Author Affiliation: Johnstone SR ( University of Virginia School of Medicine, PO Box 801394 Charlottesville VA 29908, USA.)
Abstract	Regulation of both the expression and function of connexins in the vascular wall is important during atherosclerosis. Progression of the disease state is marked by vascular smooth muscle cell (VSMC) proliferation, which coincides with the reduced expression levels of connexin 43 (Cx43). However, nothing is currently known about the factors that regulate post-translational modifications of Cx43 in atherogenesis, which could be of particular importance, due to the association between site-specific Cx43 phosphorylation and cellular proliferation. We compared the effects of direct carotid applications of two oxidized phospholipid derivatives, 1-palmitoyl-2-oxovaleroyl-sn-glycero-3-phosphorylcholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphorylcholine (PGPC), on Cx43 expression and phosphorylation, and on cell proliferation. Since both POVPC and PGPC have been shown to act through different intracellular pathways, we hypothesized that each oxidized phospholipid species could induce differential Cx43 phosphorylation events in the cytoplasmically located carboxyl-terminal region of the protein, which could potentially enhance cell proliferation. Application of POVPC caused a reduction in VSMC Cx43 levels, enhanced its phosphorylation at serine (pS) 279/282, and increased VSMC proliferation both in vivo and in vitro. Treatment with PGPC enhanced VSMC pS368 levels with no associated change in proliferation. These oxidized phospholipid-induced Cx43 post-translational changes in VSMCs were consistent with those identified in ApoE(-/-) mice. Taken together, these results demonstrate that post-translational phosphorylation of Cx43 could be a key factor in the pathogenesis of atherosclerosis.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2009.090160
Journal	The American Journal of Pathology
Issue Number	2
Volume Number	175
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2009-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Phosphorylation Phospholipid Ethers Cell Proliferation Carotid Arteries Mice, Inbred C57bl Discipline Pathology Phospholipids Connexin 43 Metabolism Pathology Muscle, Smooth, Vascular Myocytes, Smooth Muscle Animals Oxidation-reduction Atherosclerosis Protein Processing, Post-translational Genetics Apolipoproteins E Mice
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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