Lysophosphatidylcholine: Essential role in the inhibition of endothelium-dependent vasorelaxation by oxidized low density lipoprotein

Yokoyama, Mitsuhiro; Hirata, Ken–ichi; Miyake, Ryohei; Akita, Hozuka; Ishikawa, Yuichi; Fukuzaki, Hisashi

doi:10.1016/0006-291x(90)91708-z

Cited by 178 publications

(69 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…56 In cholesterol-fed animals, lyso-PC accumulates in the vessel wall, 7 -28 and lyso-PC has been found in atherosclerotic vascular lesions in humans. 28 The levels of lyso-PC in human atherosclerotic lesions are similar to those used in the present experiments (10 ^irnol/L), 6 '" although the intracellular concentration is not precisely known. It is known that lyso-PC may have nonspecific detergent-like cytotoxic properties in concentrations above those necessary to form micelles (>20 jumol/L).…”

Section: Discussionsupporting

confidence: 68%

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Ohara

Peterson

Zheng

et al. 1994

Arterioscler Thromb

126

View full text Add to dashboard Cite

We tested the hypothesis that lysophosphatidylcholine (lyso-PC) could activate protein kinase C in intact vascular segments and sought to examine some of the physiological consequences of this activation. In segments of rabbit aorta, the patterns of protein phosphorylation determined by two-dimensional electrophoresis stimulated by lyso-PC and 12-0-tetradecanoylphorbol 13-acetate (TPA) were similar. Activation of protein kinase C can stimulate superoxide anion (O 2~) production in other tissues, and we found that lyso-PCtreated rabbit aortas produced twofold more O 2~ than control vessels. Calphostin C, a potent and specific inhibitor of protein kinase C, attenuated O 2~ production in lyso-PC-treated vessels but had no effect in control vessels. The effect of lyso-PC on O 2~ production was mimicked by TPA. In separate bioassay studies, release of the endothelium-derived vascular relaxing S everal lines of evidence have indicated that oxidatively modified low-density lipoprotein (LDL) plays a central role in atherogenesis.

show abstract

Section: Discussionsupporting

confidence: 68%

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Ohara

Peterson

Zheng

et al. 1994

Arterioscler Thromb

126

View full text Add to dashboard Cite

show abstract

“…18 Oxidized LDL is known to inhibit endotheliumdependent vasodilation by increased lysophoshatidylcholine (LPC) in oxLDL. 19,20 Since LDL-C is oxidatively modified in the arterial wall and oxLDL accumulated in a local atherosclerotic lesion, increased LPC in oxLDL seems to inhibit endothelium-dependent vasodilation.…”

Section: Discussionmentioning

confidence: 99%

“…Probucol is one of the strongest antioxidant agents and has lipid-lowering effects. 20 Cote et al 8 reported that probucol reduced the restenosis rate after percutaneous old balloon angioplasty by improving CR. Thus, oxLDL may contribute to CR.…”

Section: Discussionmentioning

confidence: 99%

Oxidized low‐density lipoprotein and high‐density lipoprotein cholesterol modulate coronary arterial remodeling: An intravascular ultrasound study

Yoneyama

Arakawa

Yonemura

et al. 2003

Clinical Cardiology

View full text Add to dashboard Cite

SummaryBackground: Oxidized low-density lipoprotein (oxLDL) not only plays an important role in plaque formation, but also impairs the endothelium-dependent relaxation. Constrictive remodeling rather than intimal hyperplasia mainly contributes to restenosis after balloon angioplasty. Probucol (powerful antioxidant) reduced restenosis rate by improving constrictive remodeling. Thus, oxLDL may modulate coronary arterial remodeling.Hypothesis: The study was designed for using intravascular ultrasound to test the hypothesis that arterial constrictive remodeling (CR) was associated with oxLDL in patients with coronary artery disease.Methods: Intravascular ultrasound was performed in 36 patients with de novo atherosclerotic coronary. Remodeling was defined and evaluated as follows: remodeling index (RI) = lesion vessel area (VA)/(proximal reference VA + distal reference VA)/2. Constrictive remodeling (CR) was defined as remodeling index (RI) < 0.9. Neutral and expansive remodeling (NER) was defined as RI ≥ 0.9. The level of plasma ox-LDL was measured by sandwich ELISA using the monoclonal antibody (DLH3)-recognized oxidatively modified lipoproteins and the antihuman apoprotein B monoclonal antibody.

show abstract

“…McPherson et al, 1995 and acetylcholine in rabbit aorta Ž . Jacobs et al, 1990;Yokoyama et al, 1990 . The few studies that have shown native LDL to inhibit endothe-Ž lium-dependent relaxation Andrews et al, 1987;Galle et .…”

Section: Discussionmentioning

confidence: 99%

Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta

Grieve

Avella

Botham

et al. 1998

European Journal of Pharmacology

View full text Add to dashboard Cite

. (1998). Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta. European Journal of Pharmacology, 348(2-3)(2-3), 181-190. DOI: 10.1016181-190. DOI: 10. /S0014-2999 AbstractThe effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta were studied in vitro. Chylomicrons and chylomicron remnants were prepared in vivo. Aortic rings were incubated with the lipoproteins for 45 min before the vessels were constricted with phenylephrine and concentration relaxation response curves constructed to carbachol, ATP, A23187 and S-nitroso-N-acetylpenicillamine. Maximum % relaxations to carbachol were significantly reduced by both chylomicrons and chylomicron remnants but responses to ATP and S-nitroso-N-acetylpenicillamine were unaffected. In addition, chylomicrons significantly inhibited A23187-induced relaxation, causing an increase in the EC value. Chylomicron remnants cause selective inhibition of carbachol-induced 50 relaxation suggesting an action at the receptor or G protein-coupled component of the receptor-mediated activation of the L-arginine-nitric oxide pathway. Chylomicrons appear to be less selective in their inhibition of the endothelium-dependent relaxation. This study demonstrates that lipoprotein particles of dietary origin may cause endothelial cell dysfunction. q 1998 Elsevier Science B.V. All rights reserved. Ž .Ž .

show abstract

Lysophosphatidylcholine: Essential role in the inhibition of endothelium-dependent vasorelaxation by oxidized low density lipoprotein

Cited by 178 publications

References 10 publications

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Oxidized low‐density lipoprotein and high‐density lipoprotein cholesterol modulate coronary arterial remodeling: An intravascular ultrasound study

Effects of chylomicrons and chylomicron remnants on endothelium-dependent relaxation of rat aorta

Contact Info

Product

Resources

About