NFκB and AP-1 differentially contribute to the induction of Mn-SOD and eNOS during the development of oxidant tolerance Tao Rui and Peter R. Kvietys 1 Vascular Cell Biology Laboratory, Centre for Critical Illness Research, Lawson Health Research Institute and Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada 1 Correspondence: E-mail: pkvietys@uwo.ca <h3>SPECIFIC AIMS</h3> Exposure of cardiac myocytes to anoxia/reoxygenation (A/R) converts the myocytes to a proinflammatory phenotype, an event prevented by a previous challenge with A/R or H 2 O 2 (oxidant tolerance). Oxidant tolerance is dependent on the induction of Mn-SOD and eNOS. The aim of the present study was to assess the relative roles of the nuclear transcription factors, NFκB and AP-1 in the induction of eNOS and Mn-SOD during development of oxidant tolerance. <h3>PRINCIPAL FINDINGS</h3> <h3>1. NFκB and AP-1 are involved in the development of oxidant tolerance</h3> As the basic experimental model, cardiomyocytes were exposed to a 30 min period of anoxia, then reoxygenated (A/R). Cardiomyocytes exposed to 30 min of normoxia and reoxygenated (N/R) served as controls. An A/R challenge to cardiomyocytes induced an increase in intracellular oxidant stress (<h3>Fig. 1</h3> A) and converted the myocytes to a proinflammatory phenotype, i.e.,
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NFκB and AP-1 differentially contribute to the induction of Mn-SOD and eNOS during the development of oxidant tolerance
Rui, Tao; Kvietys, Peter R.
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, Volume 19 (13): 1908
Fed of American Socs for Experimental Biology – Nov 1, 2005
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