Linked Life Data

17999029

Source:http://linkedlifedata.com/resource/pubmed/id/17999029

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-18
pubmed:abstractText
Redox signaling prior to a lethal ischemic insult is an important step in triggering the protected state in ischemic preconditioning. When the preconditioned heart is reperfused a second sequence of signal transduction events, the mediator pathway, occurs which is believed to inhibit mitochondrial permeability transition pore formation that normally destroys mitochondria in much of the reperfused tissue. Prominent among the mediator pathway's events is activation of phosphatidylinositol 3-kinase and extracellular signal-regulated kinase. Recently it was found that both activation of PKC and generation of reactive oxygen species (ROS) at the time of reperfusion are required for protection in preconditioned hearts. To establish their relative order we tested whether ROS formation at reperfusion is required in hearts protected by direct activation of PKC at reperfusion. Isolated rabbit hearts were exposed to 30 min of regional ischemia and 2 h of reperfusion. Preconditioned hearts received 5 min of global ischemia and 10 min of reperfusion prior to the index ischemia. Another group of preconditioned hearts was exposed to 300 microM of the ROS scavenger N-(2-mercaptopropionyl) glycine (MPG) for 20 min starting 5 min prior to reperfusion. Infarct size was measured by triphenyltetrazolium staining. Preconditioning reduced infarct size from 36% +/- 2% of the ischemic zone in control hearts to only 18 +/- 2%. MPG during early reperfusion completely blocked preconditioning's protection (33 +/- 3% infarction). MPG given in the same dose and schedule to non-preconditioned hearts had no effect on infarct size. In the last group phorbol 12-myristate 13-acetate (PMA) (0.05 nM) was given to non-preconditioned hearts from 1 min before to 5 min after reperfusion in addition to MPG administered as in the other groups. MPG did not block protection from an infusion of PMA as infarct size was only 9 +/- 2% of the risk zone. We conclude that while redox signaling during the first few minutes of reperfusion is an essential component of preconditioning's protective mechanism, this step occurs upstream of PKC activation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-10720416, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-10988237, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-12200636, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-12213816, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-15173880, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-16450075, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-16545350, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-16720572, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-17350035, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-17389262, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-17450314, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-17530316, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-17632123, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-2203553, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-2548761, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-8072020, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-9040035, http://linkedlifedata.com/resource/pubmed/commentcorrection/17999029-9130455
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0300-8428
pubmed:author
pubmed:issnType
Print
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-9
pubmed:dateRevised
2010-12-3
pubmed:meshHeading
pubmed-meshheading:17999029-Analysis of Variance, pubmed-meshheading:17999029-Animals, pubmed-meshheading:17999029-Free Radical Scavengers, pubmed-meshheading:17999029-Glycine, pubmed-meshheading:17999029-Heart, pubmed-meshheading:17999029-Hemodynamics, pubmed-meshheading:17999029-Ischemic Preconditioning, Myocardial, pubmed-meshheading:17999029-Myocardial Ischemia, pubmed-meshheading:17999029-Myocardial Reperfusion, pubmed-meshheading:17999029-Myocardium, pubmed-meshheading:17999029-Oxidation-Reduction, pubmed-meshheading:17999029-Protein Kinase C, pubmed-meshheading:17999029-Rabbits, pubmed-meshheading:17999029-Reactive Oxygen Species, pubmed-meshheading:17999029-Signal Transduction, pubmed-meshheading:17999029-Sulfhydryl Compounds, pubmed-meshheading:17999029-Tetradecanoylphorbol Acetate
pubmed:year
2008
pubmed:articleTitle
Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator.
pubmed:affiliation
Department of Physiology, MSB 3074, University of South Alabama College of Medicine, Mobile, AL 36688, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural