Linked Life Data

11157669

Source:http://linkedlifedata.com/resource/pubmed/id/11157669

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Although ischemic stress, including ischemic preconditioning (IP), activates p38 mitogen-activated protein kinase (MAPK), the relationship between p38 MAPK activation and the underlying cellular mechanisms of cardioprotection by IP is not verified in vivo. We examined the effects of the selective p38 MAPK inhibition on the cardioprotective effect of IP in the open-chest dogs. The coronary artery was occluded 4 times for 5 minutes, separated by 5 minutes of reperfusion (IP) followed by 90 minutes of occlusion and 6 hours of reperfusion. We infused SB203580 into the coronary artery during IP and 1 hour of reperfusion, during IP alone, and during sustained ischemia in the IP group. p38 MAPK activity markedly increased during IP but did not additionally increase at the onset of ischemia and was even attenuated at 15 minutes of sustained ischemia, and heat-shock protein (HSP) 27 was phosphorylated and translocated from cytosol to myofibril or nucleus without affecting total protein level at the onset of ischemia compared with the control group. SB203580 treatment (1 micromol/L) only during IP blunted the infarct size limitation by IP (37.3+/-6.3% versus 7.4+/-2.1% in the IP group, P:<0.01) and attenuated either phosphorylation or translocation of HSP27 during IP. Although the SB203580 treatment throughout the preischemic and postischemic periods had no significant effect on infarct size (33.3+/-9.4%) in this model, treatment with SB203580 only during ischemia partially mimicked the infarct size limitation by IP (26.8+/-3.5%). Thus, transient p38 MAPK activation during ischemic preconditioning mainly mediates the cardioprotection followed by HSP27 phosphorylation and translocation in vivo in the canine heart.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
175-80
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11157669-Animals, pubmed-meshheading:11157669-Blotting, Western, pubmed-meshheading:11157669-Coronary Circulation, pubmed-meshheading:11157669-Disease Models, Animal, pubmed-meshheading:11157669-Dogs, pubmed-meshheading:11157669-Enzyme Activation, pubmed-meshheading:11157669-Enzyme Inhibitors, pubmed-meshheading:11157669-Heart, pubmed-meshheading:11157669-Heat-Shock Proteins, pubmed-meshheading:11157669-Hemodynamics, pubmed-meshheading:11157669-Imidazoles, pubmed-meshheading:11157669-Infusions, Intravenous, pubmed-meshheading:11157669-Ischemic Preconditioning, Myocardial, pubmed-meshheading:11157669-Mitogen-Activated Protein Kinases, pubmed-meshheading:11157669-Myocardial Infarction, pubmed-meshheading:11157669-Myocardium, pubmed-meshheading:11157669-Phosphorylation, pubmed-meshheading:11157669-Protein Transport, pubmed-meshheading:11157669-Pyridines, pubmed-meshheading:11157669-Survival Rate, pubmed-meshheading:11157669-p38 Mitogen-Activated Protein Kinases
pubmed:year
2001
pubmed:articleTitle
Role of phasic dynamism of p38 mitogen-activated protein kinase activation in ischemic preconditioning of the canine heart.
pubmed:affiliation
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't