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Journal of Lipid Research, Vol. 48, 1673-1680, August 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Review

Remnant-like lipoprotein particles impair endothelial function: direct and indirect effects on nitric oxide synthase

Xiao-Yan Zheng¹ and Ling Liu^1,2

Department of Cardiology, the Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, P.R. China

Published, JLR Papers in Press, May 13, 2007.

¹ X. Y. Zheng and L. Liu contributed equally to this work.

² To whom correspondence should be addressed. e-mail: feliuling{at}medmail.com.cn

Remnant-like lipoprotein particles (RLPs) have been implicated as potentially atherogenic lipoproteins. Endothelial dysfunction is known to be an early event in atherosclerosis and an important contributor to the pathogenesis of coronary artery disease. Moreover, there is considerable evidence linking increased RLP cholesterol levels with endothelial dysfunction, reflected by impaired endothelial vasodilatation and abnormal endothelial secretion. The underlying mechanisms by which RLPs may contribute to endothelial dysfunction are complex and have not been completely elucidated. Because the expression and activation of endothelial nitric oxide synthase (eNOS) are vital to endothelial function, and recent data have implied an association between RLPs and eNOS, this manuscript proposes the hypothesis that RLPs could impair endothelial function via direct and indirect effects on eNOS: RLPs may affect the autophosphorylation of focal adhesion kinase and its downstream phosphatidylinositol kinase/Akt (protein kinase B) signaling pathway, resulting in eNOS inactivation through induction of intracellular oxidative stress in endothelial cells; and RLPs could affect the expression or activation of eNOS indirectly by stimulating secretion of various inflammatory factors from multiple origins. The practical applications of this manuscript provide new insights for the future investigation of RLPs.

Supplementary key words endothelial dysfunction • atherosclerosis • inflammation

Abbreviations: ACh, acetylcholine; apoE, apolipoprotein E; CAD, coronary artery disease; CRP, C-reactive protein; EDR, endothelium-dependent vasorelaxation; eNOS, endothelial nitric oxide synthase; FAK, focal adhesion kinase; FMD, flow-mediated endothelium-dependent dilatation; HUVEC, human umbilical vein endothelial cell; ICAM-1, intercellular adhesion molecule-1; IL-1, interleukin-1; NO, nitric oxide; Ox-LDL, oxidized LDL; RLP, remnant-like lipoprotein particle; RLP-C, RLP-cholesterol; TNF-, tumor necrosis factor-; VCAM-1, vascular cell adhesion molecule-1

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