Source:http://linkedlifedata.com/resource/pubmed/id/15717324
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2005-6-1
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pubmed:abstractText |
The process of cardiac hypertrophy is considered to involve two components: that of cardiac myocyte (CM) enlargement and cardiac fibroblast (CF) proliferation. The interleukin-6 (IL-6) family cytokines have been implicated in a variety of cellular and molecular interactions between myocytes and non-myocytes (NCMs), which in turn have important roles in the development of cardiac hypertrophy. In the study of these interactions, we previously detected very high levels of IL-6 in supernatants of a "dedifferentiated model" of adult ventricular CMs cultured with CFs. In the present study, we have used this in vitro coculture system to examine how IL-6 is involved in the interactions between CMs and CFs during CM hypertrophy and CF proliferation. IL-6 and its signal transducer, 130-kDa glycoprotein (gp130), were detected by immunostaining cultured CMs and CFs with anti-IL-6 or anti-gp130 antibodies. Addition of anti-IL-6 or anti-gp130 antagonist antibodies into CM/CF cocultures induced a significant decrease in expression of atrial natriuretic peptide (ANP) and beta-myosin heavy chain (beta-MHC) in CMs. The presence of IL-6 antagonist also resulted in a decrease in the surface area of 12-day-old CMs cultured with CFs or in the presence of fibroblast conditioned medium (FCM), and decreased fibroblast proliferation in CM/CF cocultures, particularly in the presence of a gp130 antagonist. The results also show that angiotensin II (AngII) is mainly secreted by CFs and induces IL-6 secretion in CMs cultured with CFs or with FCM. In addition, the effects of IL-6 on cardiomyocyte hypertrophy and fibroblast proliferation were inhibited by addition of the AT-1 receptor antagonist, losartan. These results suggest that IL-6 contributes significantly to CM hypertrophy by an autocrine pathway and to fibroblast proliferation by a paracrine pathway and that these effects could be mediated by AngII.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokine Receptor gp130,
http://linkedlifedata.com/resource/pubmed/chemical/Il6st protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0021-9541
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pubmed:author | |
pubmed:copyrightInfo |
(c) 2005 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
204
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
428-36
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15717324-Angiotensin II,
pubmed-meshheading:15717324-Animals,
pubmed-meshheading:15717324-Antigens, CD,
pubmed-meshheading:15717324-Cell Proliferation,
pubmed-meshheading:15717324-Cells, Cultured,
pubmed-meshheading:15717324-Cytokine Receptor gp130,
pubmed-meshheading:15717324-Fibroblasts,
pubmed-meshheading:15717324-Hypertrophy,
pubmed-meshheading:15717324-Interleukin-6,
pubmed-meshheading:15717324-Membrane Glycoproteins,
pubmed-meshheading:15717324-Mice,
pubmed-meshheading:15717324-Myocardium,
pubmed-meshheading:15717324-Myocytes, Cardiac,
pubmed-meshheading:15717324-Receptor, Angiotensin, Type 1,
pubmed-meshheading:15717324-Tissue Distribution
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pubmed:year |
2005
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pubmed:articleTitle |
Role of interleukin-6 in cardiomyocyte/cardiac fibroblast interactions during myocyte hypertrophy and fibroblast proliferation.
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pubmed:affiliation |
Laboratoire de Physiologie et Physiopathologie Cardiaques, Université de Poitiers, Poitiers, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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