pubmed-article:15717324 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0596981 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C0020564 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:15717324 | lifeskim:mentions | umls-concept:C1326347 | lld:lifeskim |
pubmed-article:15717324 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:15717324 | pubmed:dateCreated | 2005-6-1 | lld:pubmed |
pubmed-article:15717324 | 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. | lld:pubmed |
pubmed-article:15717324 | pubmed:language | eng | lld:pubmed |
pubmed-article:15717324 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15717324 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15717324 | pubmed:month | Aug | lld:pubmed |
pubmed-article:15717324 | pubmed:issn | 0021-9541 | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:DelwailAdrian... | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:LecronJean-Cl... | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:BescondJocely... | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:PotreauDaniel... | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:FredjSandraS | lld:pubmed |
pubmed-article:15717324 | pubmed:author | pubmed-author:LouaultClaire... | lld:pubmed |
pubmed-article:15717324 | pubmed:copyrightInfo | (c) 2005 Wiley-Liss, Inc. | lld:pubmed |
pubmed-article:15717324 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15717324 | pubmed:volume | 204 | lld:pubmed |
pubmed-article:15717324 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15717324 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15717324 | pubmed:pagination | 428-36 | lld:pubmed |
pubmed-article:15717324 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:meshHeading | pubmed-meshheading:15717324... | lld:pubmed |
pubmed-article:15717324 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15717324 | pubmed:articleTitle | Role of interleukin-6 in cardiomyocyte/cardiac fibroblast interactions during myocyte hypertrophy and fibroblast proliferation. | lld:pubmed |
pubmed-article:15717324 | pubmed:affiliation | Laboratoire de Physiologie et Physiopathologie Cardiaques, Université de Poitiers, Poitiers, France. | lld:pubmed |
pubmed-article:15717324 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15717324 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:16193 | entrezgene:pubmed | pubmed-article:15717324 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:15717324 | lld:entrezgene |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15717324 | lld:pubmed |