Influence of Fe(II) and Fe(III) on the expression of genes related to cholesterol- and fatty acid metabolism in human vascular smooth muscle cells

2010 ◽  
Vol 21 (5) ◽  
pp. 1655-1663 ◽  
Author(s):  
Andreas Drynda ◽  
René Hoehn ◽  
Matthias Peuster
Keyword(s):  
Smooth Muscle ◽  
Fatty Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Muscle Cells ◽  
Expression Of Genes

Fatty acid catalytic enzymes in vascular smooth muscle cells play a crucial role in the pathogenesis of atherosclerosis

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P3264-P3264
Author(s):  
H. Matsui ◽  
T. Yokoyama ◽  
H. Sunaga ◽  
S. Anjo ◽  
T. Iso ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Fatty Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Crucial Role ◽  
Muscle Cells

Oxidant-induced arachidonic acid release and impairment of fatty acid acylation in vascular smooth muscle cells

1998 ◽  
Vol 274 (4) ◽  
pp. C1040-C1046 ◽  
Author(s):  
Agnès Cane ◽  
Michelyne Breton ◽  
Kamen Koumanov ◽  
Gilbert Béréziat ◽  
Odile Colard
Keyword(s):  
Oxidative Stress ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Atp Content

Oxidative damage, which plays a major role in the early stages of atherosclerosis, is associated with arachidonic acid (AA) release in vascular smooth muscle cells (VSMC) as in other cell types. In this study, H2O2was used to investigate mechanisms of AA release from VSMC on oxidative stress. Cell treatment with H2O2inhibited AA incorporation in an inverse relationship to prolonged H2O2-induced AA release. Identical kinetics of inhibition of AA incorporation and AA release were observed after cell treatment with A[Formula: see text], a process not involving phospholipase A2(PLA2) activation as recently described (A. Cane, M. Breton, G. Béréziat, and O. Colard. Biochem. Pharmacol. 53: 327–337, 1997). AA release was not specific, since oleic acid also increased in the extracellular medium of cells treated with H2O2or A[Formula: see text] as measured by gas chromatography-mass spectrometry. In contrast, AA and oleic acid cell content decreased after cell treatment. Oleoyl and arachidonoyl acyl-CoA synthases and acyltransferases, assayed using a cell-free system, were not significantly modified. In contrast, a good correlation was observed between decreases in AA acylation and cell ATP content. The decrease in ATP content is only partially accounted for by mitochondrial damage as assayed by rhodamine 123 assay. We conclude that oxidant-induced arachidonate release results from impairment of fatty acid esterification and that ATP availability is probably responsible for free AA accumulation on oxidative stress by preventing its reesterification and/or transmembrane transport.

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