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Am J Physiol Heart Circ Physiol (June 26, 2003). doi:10.1152/ajpheart.00416.2003
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Submitted on May 8, 2003
Accepted on June 5, 2003

Cardioprotection involves activation of NF-{kappa}B via PKC-dependent tyrosine and serine phosphorylation of I{kappa}B-{alpha}

Jun Zhang1, Peipei Ping1*, Thomas M. Vondriska1, Xian-Liang Tang2, Guang-Wu Wang1, Ernest M. Cardwell1, and Roberto Bolli2

1 Departments of Physiology and Medicine, University of California at Los Angeles, Los Angeles, CA, USA
2 Department of Medicine and Cardiology, University of Louisville, Louisville, KY, USA

* To whom correspondence should be addressed. E-mail: peipeiping{at}earthlink.net.

Previous studies have indicated that activation of protein kinase C (PKC) and Src tyrosine kinases by ischemic preconditioning (PC) may participate in the activation of nuclear factor-{kappa}B (NF-{kappa}B). However, the molecular mechanisms underlying activation of NF-{kappa}B during ischemic PC remain unknown. In the hearts of conscious rabbits, it was found that ischemic PC (six cycles of 4 min coronary occlusion/4 min reperfusion) significantly induced both tyrosine (+226.9±42%) and serine (+137.0±36%) phosphorylation of the NF-{kappa}B inhibitory protein I{kappa}B-{alpha}, concomitant with increased activation of the I{kappa}B-{alpha} kinases, IKK{alpha} (+255.0±46%) and IKK{beta} (+173.1±35%). Furthermore, both tyrosine and serine phosphorylation of I{kappa}B-{alpha} were blocked by pretreatment with either the non-receptor tyrosine kinase inhibitor lavendustin-A (LD-A) or the PKC inhibitor chelerythrine (CHE) (both given at doses previously shown to block ischemic PC). Interestingly, CHE completely abolished PC-induced activation of IKK{alpha}/{beta}, whereas LD-A had no effect. In addition, I{kappa}B-{alpha} protein level did not change during ischemic PC. Taken together, these data indicate that ischemic PC-induced activation of NF-{kappa}B occurs through both tyrosine and serine phosphorylation of I{kappa}B-{alpha} and is regulated by non-receptor tyrosine kinases and PKC.




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