Linked Life Data

11013126

Source:http://linkedlifedata.com/resource/pubmed/id/11013126

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2000-11-6
pubmed:abstractText
Cardiotrophin-1 (CT-1) is a potent cytokine that stimulates the assembly of sarcomeric units in series in cardiomyocytes through gp130 signaling, resulting in myocardial cell hypertrophy. To clarify the role of CT-1 and the gp130-signaling pathway during ventricular remodeling after myocardial infarction, we examined the expression of CT-1 and gp130 in a rat model of myocardial infarction. At 1, 3, 7, 14, 28 and 56 days (n=12 for each group) after ligation of a coronary artery, tissue samples were obtained from infarct tissue, the ventricular septum and the right ventricle. All animals developed large myocardial infarctions, with infarct sizes ranging from 39.8% to 50.3%. Progressive left ventricular dilatation and inadequate hypertrophy of the surviving myocardium were confirmed by echocardiography. CT-1 and gp130 mRNA levels were determined by semiquantitative reverse transcription-polymerase chain reaction using 1 or 5 microg of total RNA followed by Southern blotting. The densitometric analysis of the Southern blots revealed a significant increase in CT-1 and gp130 mRNA levels (P<0.01) compared with those of the sham-operated rats at 1, 3, 7, 14, 28 and 56 days post-infarct in the infarct area, the ventricular septum (non-infarcted area) and right ventricle. The protein levels of CT-1 and gp130, determined by Western blot analysis, were significantly increased (P<0.05) compared with those of sham-operated rats, peaked during the acute stage and declined thereafter in the three regions described above. Immunohistochemical staining showed that CT-1 and gp130-immunoreactivities were detected in cardiomyocytes and fibroblast-like cells and that the intensity of staining was increased at 7 days post-infarct compared with that in sham-operated rats. An augmented CT-1 and gp130 system thus appears to play an important role during ventricular remodeling after myocardial infarction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-2828
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1821-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11013126-Animals, pubmed-meshheading:11013126-Antigens, CD, pubmed-meshheading:11013126-Blotting, Southern, pubmed-meshheading:11013126-Blotting, Western, pubmed-meshheading:11013126-Coronary Vessels, pubmed-meshheading:11013126-Cytokine Receptor gp130, pubmed-meshheading:11013126-Cytokines, pubmed-meshheading:11013126-Disease Models, Animal, pubmed-meshheading:11013126-Echocardiography, pubmed-meshheading:11013126-Fibroblasts, pubmed-meshheading:11013126-Heart Ventricles, pubmed-meshheading:11013126-Immunohistochemistry, pubmed-meshheading:11013126-Membrane Glycoproteins, pubmed-meshheading:11013126-Myocardial Infarction, pubmed-meshheading:11013126-Precipitin Tests, pubmed-meshheading:11013126-RNA, Messenger, pubmed-meshheading:11013126-Rats, pubmed-meshheading:11013126-Rats, Sprague-Dawley, pubmed-meshheading:11013126-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11013126-Signal Transduction, pubmed-meshheading:11013126-Time Factors
pubmed:year
2000
pubmed:articleTitle
Augmented expression of cardiotrophin-1 and its receptor component, gp130, in both left and right ventricles after myocardial infarction in the rat.
pubmed:affiliation
Department of Cardiovascular Medicine, Kyoto University, Japan. taoyama@kuhp.kyoto-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't