Linked Life Data

16863990

Source:http://linkedlifedata.com/resource/pubmed/id/16863990

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-7-25
pubmed:abstractText
Within arterial bifurcations or branching points, oscillatory shear stress (OSS) induces oxidative stress mainly via the reduced nicotinamide adenine dinucleodtide phosphate (NADPH) oxidase system. It is unknown whether 17beta-estradiol (E(2)) can regulate OSS-mediated low-density lipoprotein (LDL) modifications. Bovine aortic endothelial cells were pretreated with E(2) at 5 nmol/L, followed by exposure to OSS (0 +/- 3.0 dynes/cm(2) s and 60 cycles/min) in a flow system. E(2) decreased OSS-mediated NADPH oxidase mRNA expression, and E(2)-mediated (.-)NO production was mitigated by the NO synthase inhibitor N(G)-nitro-l-argenine methyl ester. The rates of O(2)(-.) production in response to OSS increased steadily as determined by superoxide-dismutase-inhibited ferricytochrome c reduction; whereas, pretreatment with E(2) decreased OSS-mediated O(2)(-.) production (n = 4, p < 0.05). In the presence of native LDL (50 microg/mL), E(2) also significantly reversed OSS-mediated LDL oxidation as determined by high-performance liquid chromatography. In the presence of O(2)(-.) donor, xanthine oxidase (XO), E(2) further reversed XO-induced LDL lipid peroxidation (n = 3, p < 0.001). Mass spectra acquired in the m/z 400-1800 range, revealed XO-mediated LDL protein nitration involving tyrosine 2535 in the alpha-2 domains, whereas pretreatment with E(2) reversed nitration, as supported by the changes in nitrotyrosine intensities. Thus, E(2) plays an indirect antioxidative role. In addition to upregulation of endothelial (.-)NO synthase and downregulation of Nox4 expression, E(2) influences LDL modifications via lipid peroxidation and protein nitration.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
568-78
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16863990-Adult, pubmed-meshheading:16863990-Amino Acid Sequence, pubmed-meshheading:16863990-Animals, pubmed-meshheading:16863990-Cattle, pubmed-meshheading:16863990-Cells, Cultured, pubmed-meshheading:16863990-Chromatography, High Pressure Liquid, pubmed-meshheading:16863990-Endothelium, Vascular, pubmed-meshheading:16863990-Estradiol, pubmed-meshheading:16863990-Humans, pubmed-meshheading:16863990-Lipoproteins, LDL, pubmed-meshheading:16863990-Mass Spectrometry, pubmed-meshheading:16863990-Molecular Sequence Data, pubmed-meshheading:16863990-NADPH Oxidase, pubmed-meshheading:16863990-Nitric Oxide Synthase Type III, pubmed-meshheading:16863990-Oxidation-Reduction, pubmed-meshheading:16863990-RNA, Messenger, pubmed-meshheading:16863990-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2006
pubmed:articleTitle
17beta-Estradiol reverses shear-stress-mediated low density lipoprotein modifications.
pubmed:affiliation
Department of Biomedical Engineering and Cardiovascular Medicine, Atherosclerosis Research Unit, University of Southern California, Los Angeles, CA 90081, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural