Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-3-31
pubmed:abstractText
Lectin-like oxidized low-density lipoprotein receptor (LOX-1) is a newly identified endothelial cell surface major receptor for oxidatively modified low-density lipoprotein. Progression of arthrosclerosis in the donor organ after organ transplantation is a major problem. We hypothesized that ischemia-reperfusion induces LOX-1. After 1 h ischemia of bilateral kidneys plus 3, 6, or 12 h reperfusion, we first revealed that LOX-1 mRNA expression was increased in renal cortex and medulla at 6 h after reperfusion, which was decreased by L-arginine supplement. Plasma nitric oxide (NO) end-product nitrite plus nitrate and inducible nitric oxide synthase (NOS) expression were increased after reperfusion of 6 h. However, NOS substrate L-arginine did not augment but markedly decreased plasma NO end product, because L-arginine supplement suppressed inducible NOS expression in kidney. We hypothesized that available L-arginine is depleted by ischemia-reperfusion, leading to inducible NOS induction. Ischemia decreased L-arginine levels in kidney and L-arginine supplement increased NO end products in renal cortex in the earliest phase of reperfusion. These results disclosed for the first time that a deficiency in L-arginine by ischemia reperfusion causes uncoupling of constitutive NOS, which induces inducible NOS and LOX-1, implying why L-arginine is effective for stroke or transplantation in preventing atherosclerotic progress.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/5,6,7,8-tetrahydrobiopterin, http://linkedlifedata.com/resource/pubmed/chemical/Arginine, http://linkedlifedata.com/resource/pubmed/chemical/Biopterin, http://linkedlifedata.com/resource/pubmed/chemical/Nitrates, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Nitrites, http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Oldlr1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, LDL, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Oxidized LDL, http://linkedlifedata.com/resource/pubmed/chemical/Scavenger Receptors, Class E, http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
636-43
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:12665476-Animals, pubmed-meshheading:12665476-Arginine, pubmed-meshheading:12665476-Biopterin, pubmed-meshheading:12665476-Gene Expression Regulation, pubmed-meshheading:12665476-Kidney, pubmed-meshheading:12665476-Male, pubmed-meshheading:12665476-Nitrates, pubmed-meshheading:12665476-Nitric Oxide Synthase, pubmed-meshheading:12665476-Nitric Oxide Synthase Type II, pubmed-meshheading:12665476-Nitrites, pubmed-meshheading:12665476-RNA, Messenger, pubmed-meshheading:12665476-Rats, pubmed-meshheading:12665476-Rats, Wistar, pubmed-meshheading:12665476-Receptors, LDL, pubmed-meshheading:12665476-Receptors, Oxidized LDL, pubmed-meshheading:12665476-Reperfusion Injury, pubmed-meshheading:12665476-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:12665476-Scavenger Receptors, Class E, pubmed-meshheading:12665476-Superoxide Dismutase, pubmed-meshheading:12665476-Time Factors
pubmed:year
2003
pubmed:articleTitle
Induction of LOX-1 and iNOS expressions by ischemia-reperfusion of rat kidney and the opposing effect of L-arginine.
pubmed:affiliation
The 2nd Department of Physiology, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan. hkosaka@kms.ac.jp
pubmed:publicationType
Journal Article