Linked Life Data

15228594

Source:http://linkedlifedata.com/resource/pubmed/id/15228594

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-7-1
pubmed:abstractText
Hypoxia inducible factor (HIF-1)-1alpha is a specific, oxygen-sensitive protein that regulates the activity of HIF-1, a transcriptional factor that increases after cerebral ischemia and may either promote or prevent neuronal survival. In this study to determine whether the inducible nitric oxide synthase (iNOS) gene containing the sequence of the hypoxia-responsive enhancer (HRE) was an HIF-1 target after cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO), electrophoretic mobility shift assay (EMSA) and iNOS western blot analysis were performed in the ischemic core, in the area surrounding the infarct and in the hippocampus ipsilateral and contralateral to the lesion. In addition, both HIF-1alpha mRNA and protein expression were examined in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the insult. Our results revealed that pMCAO up-regulates iNOS protein in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the lesion, and that the activation of iNOS expression is mediated by HIF-1. Moreover, HIF-1alpha mRNA and protein levels increased in the ischemic core and in the hippocampus ipsilateral to the lesion compared with the levels obtained in the corresponding areas of sham-operated controls or in the contralateral hemisphere. Particularly in the area surrounding the ischemic core, HIF-1alpha protein accumulated during pMCAO although mRNA did not increase. Our study suggests that the activation of HIF-1 might be involved in the mechanisms whereby iNOS promotes cell survival and/or death after cerebral ischemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
368-78
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15228594-Animals, pubmed-meshheading:15228594-Brain Ischemia, pubmed-meshheading:15228594-Cell Hypoxia, pubmed-meshheading:15228594-Cells, Cultured, pubmed-meshheading:15228594-Disease Models, Animal, pubmed-meshheading:15228594-Disease Progression, pubmed-meshheading:15228594-Functional Laterality, pubmed-meshheading:15228594-Glucose, pubmed-meshheading:15228594-Hippocampus, pubmed-meshheading:15228594-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:15228594-Infarction, Middle Cerebral Artery, pubmed-meshheading:15228594-Male, pubmed-meshheading:15228594-Neurons, pubmed-meshheading:15228594-Nitric Oxide Synthase, pubmed-meshheading:15228594-Nitric Oxide Synthase Type II, pubmed-meshheading:15228594-Promoter Regions, Genetic, pubmed-meshheading:15228594-Protein Binding, pubmed-meshheading:15228594-RNA, Messenger, pubmed-meshheading:15228594-Rats, pubmed-meshheading:15228594-Rats, Sprague-Dawley, pubmed-meshheading:15228594-Rats, Wistar, pubmed-meshheading:15228594-Transcription Factors
pubmed:year
2004
pubmed:articleTitle
HIF-1alpha reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion.
pubmed:affiliation
Division of Pharmacology, Department of Neuroscience, School of Medicine, Federico II University, Naples, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't