Source:http://linkedlifedata.com/resource/pubmed/id/18560881
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
2008-6-25
|
| pubmed:abstractText |
Hypoxia-inducible transcription factor-1 (HIF-1) is the most important component of cellular and molecular adaptive responses to hypoxia. We aimed to analyze effects of systemic hypoxia and CO exposure on the oxygen-regulated alpha-subunit of HIF-1 and HIF-1-dependent vasoactive target genes in rat brain. Brains of adult Sprague-Dawley rats were investigated after incubation for 3 and 12 h under normoxia, hypoxia (8% O(2)) and CO 0.1% (n = 10 per group). Upon 3 h of exposure, hypoxia and CO-induced accumulation of HIF-1alpha protein in brain homogenates assessed by Western blot analysis. In contrast to hypoxia HIF-1alpha signals decreased markedly during 12 h-exposure to CO. By immunohistochemistry, intensive HIF-1alpha-positive staining was found in neurons of the cortex and hippocampus. Cerebral expression of vasoactive target genes adrenomedullin (ADM) and vascular endothelial growth factor (VEGF) showed up-regulation during both hypoxia and CO exposure indicating functional activation of HIF-1. Hypoxia increased ADM (P < 0.05) and VEGF mRNA levels within 3 h (P < 0.01) which persisted up to 12 h of exposure (ADM, P < 0.05; VEGF, P < 0.001). Similarly, CO inhalation led to early up-regulation of VEGF (3 h: P < 0.05; 12 h: P < 0.01), but a more delayed increase of ADM mRNA levels (3 h: n.s., 12 h: P < 0.01). We suggest that CO-induced oxygen deprivation is a potent stimulus to cerebral HIF-1-regulated hypoxic stress responses even though its effects are more transient than exposure to hypoxia.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenomedullin,
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Monoxide,
http://linkedlifedata.com/resource/pubmed/chemical/Hif1a protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoxia-Inducible Factor 1, alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/vascular endothelial growth factor...
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
1439-6319
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
104
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
95-102
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:18560881-Adrenomedullin,
pubmed-meshheading:18560881-Animals,
pubmed-meshheading:18560881-Blotting, Western,
pubmed-meshheading:18560881-Brain,
pubmed-meshheading:18560881-Carbon Monoxide,
pubmed-meshheading:18560881-Cerebrovascular Circulation,
pubmed-meshheading:18560881-Disease Models, Animal,
pubmed-meshheading:18560881-Hypoxia, Brain,
pubmed-meshheading:18560881-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:18560881-Immunohistochemistry,
pubmed-meshheading:18560881-Male,
pubmed-meshheading:18560881-RNA, Messenger,
pubmed-meshheading:18560881-Rats,
pubmed-meshheading:18560881-Rats, Sprague-Dawley,
pubmed-meshheading:18560881-Stress, Physiological,
pubmed-meshheading:18560881-Time Factors,
pubmed-meshheading:18560881-Up-Regulation,
pubmed-meshheading:18560881-Vascular Endothelial Growth Factor A
|
| pubmed:year |
2008
|
| pubmed:articleTitle |
HIF-1alpha subunit and vasoactive HIF-1-dependent genes are involved in carbon monoxide-induced cerebral hypoxic stress response.
|
| pubmed:affiliation |
Department of Pediatrics, Friedrich-Alexander-University of Erlangen-Nuremberg, Loschgestrasse 15, Erlangen, Germany.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|