Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 303, Issue 4, Pages 1152-1158Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0006-291X(03)00496-0
Keywords
proinflammatory cytokines; oxidative stress; reperfusion injury; cardiomyocytes; NF-kappa B; PDTC
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Funding
- NHLBI NIH HHS [HL68020] Funding Source: Medline
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Myocardial ischemia/reperfusion is characterized by oxidative stress and induction of proinflammatory cytokines. Interleukin (IL)-18, a member of the IL-1 family, acts as a proinflammatory cytokine, and is induced during various immune and inflammatory disorders. Therefore, in the present study we investigated whether IL-18 expression is regulated by cytokines and oxidative stress in cardiomyocytes. TNF-alpha induced rapid and sustained activation of NF-kappaB whereas H2O2 induced delayed and transient activation. Both TNF-alpha and H2O2 induced IL-18 mRNA and precursor protein in cardiornyocytes, and IL-18 release into culture supernatants. However, only TNF-alpha led to sustained expression. Expression of IL-18Rbeta, but not alpha, was induced by both agonists. TNF-alpha and H2O2 induced delayed expression of IL-18 BP. Pretreatment with PDTC attenuated TNF-alpha and H2O2 induced IL-18 and IL-18Rbeta, but not basal expression of IL-18Ralpha. These results indicate that adult cardiomyocytes express IL-18 and its receptors, and proinflammatory cytokines and oxidative stress regulate their expression via activation of NF-kappaB. Presence of both ligand and receptors suggests IL-18 impacts myocardial biology through an autocrine pathway. (C) 2003 Elsevier Science (USA). All rights reserved.
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