Linked Life Data

11960975

Source:http://linkedlifedata.com/resource/pubmed/id/11960975

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-4-18
pubmed:abstractText
Hypothermia improves resistance to ischemia in the cardioplegia-arrested heart. This adaptive process produces changes in specific signaling pathways for mitochondrial proteins and heat-shock response. To further test for hypothermic modulation of other signaling pathways such as apoptosis, we used various molecular techniques, including cDNA arrays. Isolated rabbit hearts were perfused and exposed to ischemic cardioplegic arrest for 2 h at 34 degrees C [ischemic group (I); n = 13] or at 30 degrees C before and during ischemia [hypothermic group (H); n = 12]. Developed pressure, the maximum first derivative of left ventricular pressure, oxygen consumption, and pressure-rate product (P < 0.05) recovery were superior in H compared with in I during reperfusion. mRNA expression for the mitochondrial proteins, adenine translocase and the beta-subunit of F1-ATPase, was preserved by hypothermia. cDNA arrays revealed that ischemia altered expression of 13 genes. Hypothermia modified this response to ischemia for eight genes, six related to apoptosis. A marked, near fivefold increase in transformation-related protein 53 in I was virtually abrogated in H. Hypothermia also increased expression for the anti-apoptotic Bcl-2 homologue Bcl-x relative to I but decreased expression for the proapoptotic Bcl-2 homologue bak. These data imply that hypothermia modifies signaling pathways for apoptosis and suggest possible mechanisms for hypothermia-induced myocardial protection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2200-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11960975-Animals, pubmed-meshheading:11960975-Apoptosis, pubmed-meshheading:11960975-Blotting, Northern, pubmed-meshheading:11960975-Body Temperature Regulation, pubmed-meshheading:11960975-Female, pubmed-meshheading:11960975-Heart, pubmed-meshheading:11960975-Heart Arrest, Induced, pubmed-meshheading:11960975-Hypothermia, Induced, pubmed-meshheading:11960975-Male, pubmed-meshheading:11960975-Membrane Proteins, pubmed-meshheading:11960975-Mitochondrial ADP, ATP Translocases, pubmed-meshheading:11960975-Myocardial Ischemia, pubmed-meshheading:11960975-Myocardium, pubmed-meshheading:11960975-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:11960975-Oxygen Consumption, pubmed-meshheading:11960975-Pressure, pubmed-meshheading:11960975-Protein Subunits, pubmed-meshheading:11960975-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:11960975-Proton-Translocating ATPases, pubmed-meshheading:11960975-RNA, Messenger, pubmed-meshheading:11960975-Rabbits, pubmed-meshheading:11960975-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11960975-Signal Transduction, pubmed-meshheading:11960975-Tumor Suppressor Protein p53, pubmed-meshheading:11960975-Ventricular Function, Left, pubmed-meshheading:11960975-bcl-2 Homologous Antagonist-Killer Protein, pubmed-meshheading:11960975-bcl-X Protein
pubmed:year
2002
pubmed:articleTitle
Hypothermic protection of the ischemic heart via alterations in apoptotic pathways as assessed by gene array analysis.
pubmed:affiliation
Division of Cardiology, Department of Pediatrics, University of Washington, Seattle 98195, USA. xh@u.washington.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't