期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 98, 期 14, 页码 8006-8011出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.141136098
关键词
arachidonate; linoleate; hypertension; atherosclerosis
资金
- NHLBI NIH HHS [P01 HL55798, R01 HL064937, R01 HL058115, P6-HL58418, R01-HL64937, P01 HL055798, R01-HL58115] Funding Source: Medline
12/15-lipoxygenase (LOX) activity is elevated in vascular diseases associated with impaired nitric oxide ((NO)-N-.) bioactivity, such as hypertension and atherosclerosis. In this study, primary porcine monocytes expressing 12/15-LOX, rat A10 smooth muscle cells transfected with murine 12/15-LOX, and purified porcine 12/15-LOX all consumed 'NO in the presence of lipid substrate. Suppression of LOX diene conjugation by (NO)-N-. was also found, although the lipid product profile was unchanged:NO consumption by porcine monocytes was inhibited by the LOX inhibitor, eicosatetraynoic acid. Rates of arachidonate (AA)- or linoleate (LA)-dependent (NO)-N-. depletion by porcine monocytes (2.68 +/- 0.03 nmol . min(-1). 10(6) cells(-1) and 1.5 +/- 0.25 nmol min(-1). 10(6) cells(-1), respectively) were several-fold greater than rates of'tdO generation by cytokine-activated macrophages (0.1-0.2 nmol . min(-1). 10(6) cells(-1)) and LA-dependent (NO)-N-. consumption by primary porcine monocytes inhibited (NO)-N-. activation of soluble guanylate cyclase. These data indicate that catalytic (NO)-N-. consumption by 12/15-LOX modulates monocyte (NO)-N-. signaling and suggest that LOXs may contribute to vascular dysfunction not only by the bioactivity of their lipid products, but also by serving as catalytic sinks for (NO)-N-. in the vasculature.
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