rdf:type |
|
lifeskim:mentions |
umls-concept:C0001554,
umls-concept:C0031727,
umls-concept:C0100748,
umls-concept:C0205216,
umls-concept:C0205234,
umls-concept:C0205374,
umls-concept:C0205421,
umls-concept:C0332281,
umls-concept:C0599946,
umls-concept:C0917798,
umls-concept:C1159864,
umls-concept:C1879547
|
pubmed:issue |
5
|
pubmed:dateCreated |
2009-11-25
|
pubmed:abstractText |
Focal cerebral ischemia and reperfusion initiates complex cellular and molecular interactions that lead to either cell repair or destruction. In earlier work, we found that activin A is an early gene response to cerebral ischemia and supports cortical neuron survival in vitro. In this study, the ability of exogenous activin A to attenuate injury from transient middle cerebral artery occlusion was tested in adult mice. Intracerebroventricular administration of activin A prior to middle cerebral artery occlusion reduced infarct volume apparent 1 day after experimental stroke. A single activin A administration at 6 h following ischemia/reperfusion reduced lesion volumes at 1 and 3 days and led to improved neurobehavior. Moreover, activin A treatment spared neurons within the ischemic hemisphere and led to a concomitant reduction in microglial activation. Activation of the stress-responsive kinases p38 and c-jun N-terminal kinase implicated in neuronal apoptosis after stroke was reduced following activin A treatment. Together these findings suggest that activin A promotes tissue survival after focal cerebral ischemia/reperfusion with an extended therapeutic window.
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pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19780899-10392842,
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1471-4159
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pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:volume |
111
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1138-48
|
pubmed:dateRevised |
2010-9-28
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pubmed:meshHeading |
pubmed-meshheading:19780899-Humans,
pubmed-meshheading:19780899-Animals,
pubmed-meshheading:19780899-Mice,
pubmed-meshheading:19780899-Rats,
pubmed-meshheading:19780899-Neurons,
pubmed-meshheading:19780899-Injections, Intraventricular,
pubmed-meshheading:19780899-Male,
pubmed-meshheading:19780899-Infarction, Middle Cerebral Artery,
pubmed-meshheading:19780899-Time Factors,
pubmed-meshheading:19780899-Disease Models, Animal,
pubmed-meshheading:19780899-Blood Gas Analysis
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