Linked Life Data

14674704

Source:http://linkedlifedata.com/resource/pubmed/id/14674704

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-12-16
pubmed:abstractText
Cardiotrophin-1 (CT-1), a member of the IL-6 family of cytokines, has been shown to be elevated in the serum of patients with ischemic heart disease and valvular heart disease, and induces cardiomyocyte hypertrophy in vitro. We investigated expression of CT-1 in post-MI rat heart and the effect of CT-1 on cultured primary adult rat cardiac fibroblasts. Elevated CT-1 expression was observed in the infarct zone at 24 h and continued through 2, 4 and 8 weeks post-MI, compared to sham-operated animals. CT-1 induced rapid phosphorylation of Jak, Jak2, STAT1, STAT3, p42/44 MAPK and Akt in cultured adult cardiac fibroblasts. CT-1 induced cardiac fibroblast protein synthesis and proliferation. Protein and DNA synthesis were dependent on activation of Jak/STAT, MEK1/2, PI3K and Src pathways as evidenced by decreased 3H-leucine and 3H-thymidine incorporation after pretreatment with AG490, PD98059, LY294002 and genistein respectively. Furthermore, CT-1 treatment increased procollagen-1-carboxypropeptide (PICP) synthesis, a marker of mature collagen synthesis. CT-1 induced cell migration of rat cardiac fibroblasts. Our results suggest that CT-1, as expressed in post-MI heart, may play an important role in infarct scar formation and ongoing remodeling of the scar. CT-1 was able to initiate each of the processes considered important in the formation of infarct scar including cardiac fibroblast migration as well as fibroblast proliferation and collagen synthesis. Further work is required to determine factors that induce CT-1 expression and interplay with other mediators of cardiac infarct wound healing in the setting of acute cardiac ischemia and chronic post-MI heart failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
254
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
247-56
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14674704-Animals, pubmed-meshheading:14674704-Blotting, Western, pubmed-meshheading:14674704-Cell Division, pubmed-meshheading:14674704-Cell Movement, pubmed-meshheading:14674704-Cells, Cultured, pubmed-meshheading:14674704-Collagen, pubmed-meshheading:14674704-Cytokines, pubmed-meshheading:14674704-DNA, pubmed-meshheading:14674704-Disease Models, Animal, pubmed-meshheading:14674704-Dose-Response Relationship, Drug, pubmed-meshheading:14674704-Enzyme Inhibitors, pubmed-meshheading:14674704-Fibroblasts, pubmed-meshheading:14674704-Interleukin-6, pubmed-meshheading:14674704-Male, pubmed-meshheading:14674704-Mitogen-Activated Protein Kinases, pubmed-meshheading:14674704-Myocardial Infarction, pubmed-meshheading:14674704-Phosphorylation, pubmed-meshheading:14674704-Procollagen, pubmed-meshheading:14674704-Rats, pubmed-meshheading:14674704-Rats, Sprague-Dawley, pubmed-meshheading:14674704-Signal Transduction, pubmed-meshheading:14674704-Time Factors, pubmed-meshheading:14674704-Wound Healing
pubmed:year
2003
pubmed:articleTitle
Cardiotrophin-1: expression in experimental myocardial infarction and potential role in post-MI wound healing.
pubmed:affiliation
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't