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1 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA
2 Department of Internal Medicine, University of Iowa, Iowa City, IA, USA; Department of Free Radical and Radiation Biology Program, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: francis-miller{at}uiowa.edu.
Reactive oxygen species (ROS) derived from vascular NADPH oxidase are important in normal and pathologic regulation of vessel growth and function. Cell specific differences in expression and function of the catalytic subunit of NADPH oxidase may contribute to differences in vascular cell response to NADPH oxidase activation. We examined the functional expression of gp91phox on NADPH oxidase activity in vascular smooth muscle cells (SMC) and fibroblasts (FB). As measured by dihydroethidium fluorescence in situ, superoxide (O2.-) levels were greater in adventitial cells, as compared to medial SMC, in wild-type aorta. In contrast, there was no difference in O2.- levels between adventitial cells and medial SMC in aorta from gp91phox deficient (gp91phox ko) mice. Adventitial-derived FB and medial SMC were isolated from the aorta of wild type and gp91phox ko mice and grown in culture. Consistent with the observations in situ, basal and stimulated ROS levels were reduced in FB isolated from aorta of gp91phox ko compared to FB from wild-type aorta, whereas ROS levels were similar in SMC derived from gp91phox ko and wild-type aorta. There were no differences in expression of superoxide dismutase between gp91phox ko and wild-type FB to account for these observations. Since gp91phox is associated with membranes, we examined NADPH-stimulated O2.- production in membrane-enriched fractions of cell lysate. As measured by chemiluminescence, NADPH oxidase activity was markedly greater in wild-type FB compared to gp91phox ko FB, but did not differ between the SMCs. Confirming functional expression of gp91phox in FB, antisense to gp91phox decreased ROS levels in wild-type FB. Finally, deficiency of gp91phox did not alter expression of the gp91phox homologue NOX4 in isolated FB. We conclude that the neutrophil subunit gp91phox contributes to NADPH oxidase function in vascular FB, but not SMC.
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