Abstract
IntroductionOsteopontin (OPN) is involved in ectopic calcification. Its circulating form is upregulated in coronary artery disease (CAD) patients. Circulating OPN levels positively correlate with oxidative stress, one of the major triggers of endothelial dysfunction. Endothelial dysfunction is, in turn, associated with reduced nitric oxide (NO) bioavailability due to the impaired arginine pathway. The aim of this study was to better understand the correlations between OPN, oxidative stress markers, and the arginine pathway metabolites.Methods and ResultsELISA and mass spectrometry techniques have been used to evaluate circulating OPN and arginine pathway/oxidative stress metabolites, respectively, in twenty-five control subjects and thirty-three patients with overt atherosclerosis. OPN positively correlates with 2,3-dinor-8isoPGF2a levels (p = 0.02), ornithine (p = 0.01), ADMA (p = 0.001), SDMA (p = 0.03), and citrulline (p = 0.008) levels only in CAD patients. In addition, citrulline positively correlated with ADMA (p = 0.02) levels, possibly as result of other sources of citrulline biosynthetic pathways.ConclusionThe association between OPN and impaired arginine/NO pathway could play a role in the inhibition of endothelial NO synthase (eNOS) and/or in the arginase activation in the context of CAD patients. However, further studies are needed to verify the cause-effect relationship between OPN, oxidative stress, and arginine/NO pathway dysregulation.
Highlights
Osteopontin (OPN) is involved in ectopic calcification
We assess the possible relationship between OPN levels and oxidative stress status, represented by 2,3-dinor-8isoPGF2a and the ratio between the reduced (GSH) and the oxidized (GSSG) forms of glutathione, in patients before the surgical intervention
Linear regression analysis reported that there was no significant association between OPN levels and GSH/GSSG ratio, in controls, as well as in coronary artery disease (CAD) patients
Summary
Osteopontin (OPN) is involved in ectopic calcification. Its circulating form is upregulated in coronary artery disease (CAD) patients. Circulating OPN levels positively correlate with oxidative stress, one of the major triggers of endothelial dysfunction. Circulating OPN has been proposed as a predictor of major cardiac events, such as acute myocardial infarction and ischemic heart disease (Georgiadou et al, 2010; Okyay et al, 2011). These observations, taken together with large literature evidences, corroborate the direct link between OPN and CAD development/progression (Wolak, 2014). Circulating OPN positively correlates with malondialdehyde levels, a recognized biomarker of oxidative stress (Cavalca et al, 2001; Georgiadou et al, 2008)
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