期刊论文详细信息
Cardiac myocytes produce interleukin-6 in culture and in viable border zone of reperfused infarctions
Article
关键词: ACUTE MYOCARDIAL-INFARCTION;    INTERCELLULAR-ADHESION MOLECULE-1;    ISCHEMIC CANINE MYOCARDIUM;    NECROSIS-FACTOR-ALPHA;    NEUTROPHIL ADHERENCE;    NITRIC-OXIDE;    BLOOD-FLOW;    INJURY;    INDUCTION;    IL-6;   
DOI  :  10.1161/01.CIR.99.4.546
来源: SCIE
【 摘 要 】

Background-Previous work from our laboratory demonstrated that interleukin (IL)-6 plays a potentially critical role in postreperfusion myocardial injury and is the major cytokine responsible fur induction of intracellular adhesion molecule (ICAM)-1 on cardiac myocytes during reperfusion. Myocyte ICAM-1 induction is necessary for neutrophil-associated myocyte injury. We have previously demonstrated the induction of IL-6 in the ischemic myocardium, and the current study addresses the cells of origin of IL-6. Methods and Results-In the present study, we combined Northern blot analysis and in situ hybridization to demonstrate IL-6 gene expression in cardiac myocytes. Isolated ventricular myocytes were stimulated with tumor necrosis factor-alpha, IL-1 beta, lipopolysaccharide, preischemic lymph, and postischemic lymph. Unstimulated myocytes showed no significant IL-6 mRNA expression, Myocytes stimulated with preischemic lymph showed minimal or no IL-6 mRNA expression, whereas myocytes stimulated with tumor necrosis factor-alpha, IL-1 beta, lipopolysaccharide, or postischemic lymph showed a strong IL-6 mRNA induction. Northern blot with ICAM-1 probe revealed ICAM-1 expression under every condition that demonstrated IL-6 induction. We then investigated the expression of IL-6 mRNA in our canine model of ischemia and reperfusion. Cardiac myocytes in the viable border zone of a myocardial infarction exhibited reperfusion-dependent expression of IL-6 mRNA within 1 hour after reperfusion, Mononuclear cells infiltrate the border zone and express IL-6 mRNA. Conclusions-Isolated cardiac myocytes produce IL-6 mRNA in response to several cytokines as well as postischemic cardiac lymph. In addition to its production by inflammatory cells, we demonstrate that IL-6 mRNA is induced in myocytes in the viable border zone of a myocardial infarct. The potential roles of IL-6 in cardiac myocytes in an infarct border are discussed.

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