期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 47, 期 8, 页码 1140-1146出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2009.07.025
关键词
Fibrinogen; Nitration; Intima-medial thickness; Coronary artery calcification; High-density lipoprotein (HDL)
资金
- Clinical and Translational Science Award [RFA-RM-06-002]
- General Clinical Research Center [M01 RR00040]
- NCRR/NIH to the University of Pennsylvania
- Special Center of Research in Atherosclerosis [P50 HL70128]
- NHLBI/NIH [HL P50-083799]
- Doris Duke Clinical Research Fellow
- W.W. Smith Charitable Trust [H0204]
- National Institutes of Health [P50-083799, P01 HL 079063, ES013508]
- NIEHS Center of Excellence in Environmental Toxicology
- [HL RO1-073278]
- [K23 HL077146]
Elevated plasma fibrinogen is a prothrombotic risk factor for cardiovascular disease (CVD). Recent small studies report that fibrinogen oxidative modi. cations, specifically tyrosine residue nitration, can occur in inflammatory states and may modify fibrinogen function. HDL cholesterol is inversely related to CVD and suggested to reduce the oxidation of LDL cholesterol, but whether these antioxidant functions extend to fibrinogen modi. cations is unknown. We used a recently validated ELISA to quantify nitrated fibrinogen during experimental human endotoxemia (N = 23) and in a cohort of healthy adults (N = 361) who were characterized for inflammatory and HDL parameters as well as subclinical atherosclerosis measures, carotid artery intima-medial thickness (IMT) and coronary artery calcification (CAC). Fibrinogen nitration increased following endotoxemia and directly correlated with accelerated ex vivo plasma clotting velocity. In the observational cohort, nitrated fibrinogen was associated with levels of CRP and serum amyloid A. Nitrated fibrinogen levels were not lower with increasing HDL cholesterol and did not associate with IMT and CAC. In humans, fibrinogen nitration was induced during inflammation and was correlated with markers of inflammation and clotting function but not HDL cholesterol or subclinical atherosclerosis in our modest sample. Inflammation-induced fibrinogen nitration may be a risk factor for promoting CVD events. (C) 2009 Elsevier Inc. All rights reserved.
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