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1 Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
* To whom correspondence should be addressed. E-mail: cleffler{at}physio1.utmem.edu.
Carbon monoxide (CO) is produced from heme by heme oxygenase -2 (HO-2) in cerebral blood vessels. Piglet cerebral microvessels and gas chromatography/mass spectrometry were used to address the hypothesis that CO production is regulated by heme delivery and HO-2 catalytic activity. CO production appears to be substrate limited because heme and its precursor, aminolevulinate, increased CO production. Ionomycin increased CO production. However, CO production from exogenous heme was the same in Ca replete medium, Ca free medium with ionomycin, and Ca replete medium with ionomycin. Phorbol myristate acetate increased CO production but did not change the catalytic activity of HO-2. Further, the protein kinases C inhibitor, H-7, had no effect on the HO-2 catalytic activity. Protein tyrosine kinase inhibition reduced HO-2 catalytic activity. Inhibition of protein tyrosine phosphatases increased HO-2 catalytic activity. Therefore, regulation of CO production by cerebral microvessels can include changing heme availability and HO-2 catalytic activity. HO-2 catalytic activity is stimulated by tyrosine phosphorylation.
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