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Abstract
Atherosclerosis is a systemic disease, and its development is dependent upon a complex interplay among numerous genetic, epigenetic, and environmental risk factors. It is increasingly recognized that ambient UFP exposure promotes vascular oxidative stress and inflammatory responses. In this study, we tested the hypothesis that UFP attenuates eNOS activity via S‐glutathionylaiton. Treatment of human aortic endothelial cells (HAEC) with ambient UFP (Dp<100nm) significantly inhibited nitric oxide (NO) production as measured by Griess assay (Control: 3.645, UFP: 1.662, P<.01, n=4). To assess whether oxidative stress induced eNOS uncoupling via S‐glutathionylation, we demonstrated that UFP treatment increased eNOS S‐glutathionylation in HAEC by a modified ELISA procedure. To inhibit S‐glutahionylation, we over‐expressed glutaredoxin‐1 (Grx‐1), and showed a significant attenuation of UFP‐mediated decrease in NO production (LacZ+UFP: .338, Grx1+UFP: .630, P<.01, n=6). Thus, our findings suggest that UFP inhibited eNOS activity via an increase in S‐ glutathionylation.
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