Linked Life Data

16183734

Source:http://linkedlifedata.com/resource/pubmed/id/16183734

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-11
pubmed:abstractText
Transforming growth factor-beta1 (TGF-beta1) alters myocardial gene expression, resulting in myocyte hypertrophy, through activation of TGF-beta-activated kinase (TAK1), a member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family. We hypothesized that the TGF-beta1-TAK1-p38 MAPK pathway might be activated during ventricular remodeling after myocardial infarction (MI). One, 3, 7, and 14 days after ligation of the left anterior descending coronary artery, noninfarcted left ventricular tissue samples were obtained. Protein levels as well as mRNA levels of the signaling pathway, TGF-beta1, TGF-beta-receptors, and TAK1 increased in the noninfarcted myocardium in MI rats compared with sham-operated animals. Phosphorylation of MAPKK 3/6 (MKK3/6) and p38 MAPK, the downstream targets of TAK1, was also increased in the noninfarcted region. Moreover, an in vitro kinase assay revealed that the activated TAK1 in the noninfarcted myocardium was capable of activating recombinant MKK3/6, suggesting a causative role of TAK1 in the remodeling process. The activation of the TGF-beta1-TAK1-p38 MAPK pathway paralleled the transcriptional upregulation of cardiac markers for ventricular hypertrophy, beta-myosin heavy chain and atrial natriuretic peptide. TAK1 was mainly localized to cardiomyocytes, whereas TGF-beta1 receptors were observed in vascular smooth muscle cells and fibroblasts as well as cardiomyocytes. Thus the TGF-beta1-TAK1-MKK3/6-p38 MAPK pathway in the cardiomyocytes of noninfarcted spared myocardium is activated after acute MI and may play an important role in ventricular hypertrophy and post-MI remodeling in rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H709-15
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:16183734-Animals, pubmed-meshheading:16183734-Blotting, Western, pubmed-meshheading:16183734-Body Weight, pubmed-meshheading:16183734-Echocardiography, pubmed-meshheading:16183734-Enzyme Activation, pubmed-meshheading:16183734-Hemodynamics, pubmed-meshheading:16183734-Immunohistochemistry, pubmed-meshheading:16183734-MAP Kinase Kinase Kinases, pubmed-meshheading:16183734-Male, pubmed-meshheading:16183734-Myocardial Infarction, pubmed-meshheading:16183734-Myocardium, pubmed-meshheading:16183734-Myocytes, Cardiac, pubmed-meshheading:16183734-Organ Size, pubmed-meshheading:16183734-RNA, Messenger, pubmed-meshheading:16183734-Rats, pubmed-meshheading:16183734-Rats, Sprague-Dawley, pubmed-meshheading:16183734-Transforming Growth Factor beta, pubmed-meshheading:16183734-Transforming Growth Factor beta1, pubmed-meshheading:16183734-Ventricular Remodeling, pubmed-meshheading:16183734-p38 Mitogen-Activated Protein Kinases
pubmed:year
2006
pubmed:articleTitle
Activation of TGF-beta1-TAK1-p38 MAPK pathway in spared cardiomyocytes is involved in left ventricular remodeling after myocardial infarction in rats.
pubmed:affiliation
Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't