Source:http://linkedlifedata.com/resource/pubmed/id/19782128
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2010-6-14
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| pubmed:abstractText |
Apoptosis-related mechanisms are important in the pathophysiology of hypoxic-ischemic injury in the neonatal brain. Caspases are the major executioners of apoptosis, but there are a number of upstream players that influence the cell death pathways. The Bcl-2 family proteins are important modulators of mitochondrial permeability, working either to promote or prevent apoptosis. In this study we focused on the anti-apoptotic Bcl-2 protein after neonatal cerebral hypoxia-ischemia (HI) in 8-day-old rats. Bcl-2 translocated to nuclei and accumulated there over the first 24h of reperfusion after HI, as judged by immunohistochemistry and immuno-electron microscopy. We also found that the total level of Bcl-2 decreased after HI in vivo and after ionophore challenge in cultured human neuroblastoma (IMR-32) cells in vitro. Furthermore, the Bcl-2 reduction was calpain-dependent, because it could be prevented by the calpain inhibitor CX295 both in vivo and in vitro, suggesting cross-talk between excitotoxic and apoptotic mechanisms.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
1090-2139
|
| pubmed:author |
pubmed-author:BahrBen ABA,
pubmed-author:BlomgrenKlasK,
pubmed-author:GatzinskyKlimentK,
pubmed-author:GrandérRitaR,
pubmed-author:HagbergHenrikH,
pubmed-author:HallinUlrikaU,
pubmed-author:KarlssonJan-OlofJO,
pubmed-author:OzakiYasuhikoY,
pubmed-author:ShibasakiFutoshiF,
pubmed-author:ZhuChanglianC
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| pubmed:copyrightInfo |
Copyright 2009 Elsevier Inc. All rights reserved.
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| pubmed:issnType |
Electronic
|
| pubmed:volume |
24
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
822-30
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| pubmed:meshHeading |
pubmed-meshheading:19782128-Active Transport, Cell Nucleus,
pubmed-meshheading:19782128-Analysis of Variance,
pubmed-meshheading:19782128-Animals,
pubmed-meshheading:19782128-Animals, Newborn,
pubmed-meshheading:19782128-Apoptosis,
pubmed-meshheading:19782128-Blotting, Western,
pubmed-meshheading:19782128-Calpain,
pubmed-meshheading:19782128-Cell Line, Tumor,
pubmed-meshheading:19782128-Cell Nucleus,
pubmed-meshheading:19782128-Cells, Cultured,
pubmed-meshheading:19782128-Female,
pubmed-meshheading:19782128-Humans,
pubmed-meshheading:19782128-Hypoxia-Ischemia, Brain,
pubmed-meshheading:19782128-Immunohistochemistry,
pubmed-meshheading:19782128-Male,
pubmed-meshheading:19782128-Microscopy, Immunoelectron,
pubmed-meshheading:19782128-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:19782128-Rats,
pubmed-meshheading:19782128-Rats, Wistar,
pubmed-meshheading:19782128-bcl-2-Associated X Protein
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Nuclear translocation and calpain-dependent reduction of Bcl-2 after neonatal cerebral hypoxia-ischemia.
|
| pubmed:affiliation |
Center for Brain Repair and Rehabilitation, University of Gothenburg, Gothenburg, Sweden.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|