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Vol. 299, Issue 2, 477-482, November 2001
1-Opioid Receptor-Induced
Cardioprotection on a Tyrosine Kinase-Dependent but Not a Src-Dependent
Pathway
Department of Pharmacology and Toxicology, Medical College of
Wisconsin, Milwaukee, Wisconsin (R.M.F., A.K.H., G.J.G.); Department of
Pathology, University of Cincinnati College of Medicine, Cincinnati,
Ohio (Y.W.); and Toray Industries, Kanagawa, Japan (H.N.)
We investigated the possibility that opioids activate a tyrosine kinase
(TK) that mediates cardioprotection in an in vivo rat model of
myocardial infarction. All animals underwent 30 min of regional
ischemia and 2 h of reperfusion. Infarct size was expressed as a
percentage of the area at risk (IS/AAR). Control animals had an IS/AAR
of 58.2 ± 0.6. Cardioprotection was induced with the
1- or 1/2-selective opioid
agonists, TAN-67, or D-Ala D-Leu enkephalin
(DADLE). Both significantly reduced IS/AAR (28.8 ± 3.6 and
34.8 ± 3.8, respectively). The general TK inhibitor, genistein,
abolished cardioprotection produced by TAN-67 or DADLE (59.1 ± 3.2 and 61.5 ± 3.4, respectively), whereas the structural analog,
daidzein, lacking TK inhibitory activity, did not. Interestingly, the
selective Src/epidermal growth factor (EGF) receptor TK inhibitor, lavendustin A, did not abolish TAN-67-induced cardioprotection (22.1 ± 6.8). Similarly, the Src-selective TK antagonist, PP2, had no effect on DADLE-induced cardioprotection (31.1 ± 7.3). These unexpected findings suggest that Src and EGF receptor TKs are not
important in the genesis of cardioprotection produced by TAN-67.
Finally, we demonstrate that genistein did not affect protein kinase C
(PKC) translocation induced by TAN-67. These data suggest that a TK,
but most likely not an Src/EGF receptor TK, is important in
cardioprotection via opioid receptor stimulation and that the pathway
for TK activation is downstream from or parallel to PKC activation in
the in situ rat heart since genistein could not affect PKC
translocation of selective isoforms induced by TAN-67 and assessed by immunohistochemistry.
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