Source:http://linkedlifedata.com/resource/pubmed/id/17920049
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2007-11-5
|
pubmed:abstractText |
Hypoxia inducible factor-1alpha (HIF-1alpha) plays an important role in maintaining oxygen equilibrium. Pathologic conditions such as hypoxia or ischemia have been reported to cause cellular apoptosis as well as to regulate HIF-1alpha. However, the relationship between HIF-1alpha and neuronal apoptosis in neonatal rats with hypoxia-ischemia brain injury is unclear. We hypothesized that HIF-1alpha will be differentially regulated depending upon the stimuli, such as hypoxia alone versus hypoxia-ischemia (HI), and thus play a role in neuronal apoptosis in developing rat brain. To test this hypothesis, we subjected postnatal day 10 (P10) rats to either hypoxia (8%O(2) and 92%N(2) for 2.5 h) or HI (ligating the right common carotid artery followed by hypoxia). Rat brains from hypoxia, HI, and sham controls were collected to detect HIF-1alpha expression and cellular apoptosis using immunohistochemistry, Western blot analysis, and TdT-mediated dUTP-biotin nick end labeling (TUNEL). We found that HIF-1alpha expression was upregulated at 4 h, peaked at 8 h, and declined at 24 h after hypoxia/HI compared with sham controls. Moreover, HIF-1alpha expression was significantly stronger in hypoxia-alone-treated rats than that in HI-treated rats. Meanwhile, we found that cellular apoptosis was more severe in HI-treated rats than that in hypoxia-treated rats. Furthermore, cellular apoptosis was prominent at 24 h in either hypoxia or HI but more severe in HI-treated rats. Our findings that cellular apoptosis increases with downregulation of HIF-1alpha suggest that HIF-1alpha may play a protective role in regulating cellular apoptosis in neonatal hypoxia-ischemia brain damage (HIBD).
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
0006-8993
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
14
|
pubmed:volume |
1180
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
133-9
|
pubmed:meshHeading |
pubmed-meshheading:17920049-Animals,
pubmed-meshheading:17920049-Animals, Newborn,
pubmed-meshheading:17920049-Apoptosis,
pubmed-meshheading:17920049-Brain Injuries,
pubmed-meshheading:17920049-Caspase 3,
pubmed-meshheading:17920049-Cerebral Cortex,
pubmed-meshheading:17920049-Down-Regulation,
pubmed-meshheading:17920049-Female,
pubmed-meshheading:17920049-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:17920049-Hypoxia-Ischemia, Brain,
pubmed-meshheading:17920049-Male,
pubmed-meshheading:17920049-Neurons,
pubmed-meshheading:17920049-Rats,
pubmed-meshheading:17920049-Rats, Sprague-Dawley,
pubmed-meshheading:17920049-Time Factors
|
pubmed:year |
2007
|
pubmed:articleTitle |
Relationship between HIF-1alpha expression and neuronal apoptosis in neonatal rats with hypoxia-ischemia brain injury.
|
pubmed:affiliation |
Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|