TNF-alpha as a potential mediator of cardiac dysfunction due to intracellular Ca2+-overload

TNF-alpha has been shown to be involved in cardiac dysfunction during ischemia/reperfusion injury; however, no information regarding the status of TNF-alpha production in myocardial injury due to intracellular Ca2+-overload is available in the literature. The intracellular Ca2+-overload was induced...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-02, Vol.327 (1), p.57-63
Main Authors: Zhang, Ming, Xu, Yan-Jun, Saini, Harjot K, Turan, Belma, Liu, Peter P, Dhalla, Naranjan S
Format: Article
Language:English
Subjects:
Animals
Calcium - pharmacology
Heart - drug effects
Heart Diseases - metabolism
Heart Diseases - physiopathology
Male
Myocardium - metabolism
NF-kappa B - metabolism
Phosphorylation
Rats
Rats, Sprague-Dawley
Tumor Necrosis Factor-alpha - biosynthesis
Tumor Necrosis Factor-alpha - metabolism
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Summary:TNF-alpha has been shown to be involved in cardiac dysfunction during ischemia/reperfusion injury; however, no information regarding the status of TNF-alpha production in myocardial injury due to intracellular Ca2+-overload is available in the literature. The intracellular Ca2+-overload was induced in the isolated rat hearts subjected to 5 min Ca2+-depletion and 30 min Ca2+-repletion (Ca2+-paradox). The Ca2+-paradox hearts exhibited a dramatic depression in left ventricular developed pressure, a marked elevation in left ventricular end diastolic pressure, and more than a 4-fold increase in TNF-alpha content. The ratio of cytosolic to homogenate nuclear factor-kappaB (NFkappaB) was decreased whereas the ratio of phospho-NFkappaB to total NFkappaB was increased in the Ca2+-paradox hearts. All these changes due to Ca2+-paradox were significantly attenuated upon treating the hearts with 100 microM pentoxifylline. These results suggest that activation of NFkappaB and increased production of TNF-alpha may play an important role in cardiac injury due to intracellular Ca2+-overload.
ISSN:0006-291X
DOI:10.1016/j.bbrc.2004.11.131