Abstract
Trivalent chromium (Cr) is proposed to have a therapeutic potential in glycemic and cardiovascular health. While emerging evidence support a protective role of Cr in atherosclerosis, the underlying mechanisms of Cr action in diabetic vascular disease remain unknown. Diabetic patients have increased incidence of vascular smooth muscle cell (VSMC) migration and proliferation, key events leading to initiation and development of atherosclerosis. The present study provides the first evidence that Cr inhibits high glucose (30mM) induced migration and proliferation of human aortic SMC (HASMC) coupled to attenuation of ERK1/2 phosphorylation. We showed earlier that Cr downregulates a potent proatherogenic matricellular protein Thrombospondin‐1 (TSP‐1), known to accelerate initiation of atherosclerosis, concomitant to a decrease in protein O‐glycosylation. We now further demonstrate that this decrease in TSP‐1 expression is accompanied by reduction in expression of Glutamine: fructose‐6‐phosphate amidotransferase (GFAT), the key rate limiting enzyme of hexosamine pathway of glucose metabolism. Additionally, we found that Cr inhibits high glucose‐induced oxidative stress via reduction in cellular reactive oxygen species (ROS). Together, these data suggest TSP‐1 as a potential therapeutic target of Cr and provide a novel anti‐atherogenic mechanism for Cr in diabetic atherosclerotic complications.
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