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Chromium inhibits phenotypic switching of vascular smooth muscle cells in response to hyperglycemic conditions in vitro (1076.8)
Author(s) -
Ganguly Rituparna,
Sahu Soumyadip,
Boyer Brooke,
Raman Priya
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1076.8
Subject(s) - vascular smooth muscle , medicine , endocrinology , diabetes mellitus , chemistry , matricellular protein , cancer research , biology , microbiology and biotechnology , extracellular matrix , smooth muscle
Hyperglycemia is an independent risk‐factor for macrovascular complications accounting for increased morbidity and mortality in diabetes. Diabetic patients have increased incidence of vascular smooth muscle cell (VSMC) migration and proliferation attributing to accelerated macrovascular lesion development. We recently showed that trivalent chromium (Cr), a beneficial mineral nutrient, reduces high glucose‐induced expression of thrombospondin‐1 (TSP‐1), a potent proatherogenic matricellular protein implicated in atherosclerosis. Here we show that Cr specifically inhibits high glucose induced proliferation of human aortic SMC (HASMC) vs. serum‐stimulated proliferation via attenuated ERK activation. Further in glucose‐sitmulated cells using protein‐DNA array we demonstrate that Cr reduces activation of transcription factors including SP1, ELK1, YY1, known repressors of SMC contractile gene expression. In parallel, Cr increases activation of SRF, a known transcriptional activator of contractile marker, α‐SMA. Finally, Cr’s antiproliferative effect was attenuated in TSP‐1 transgenic (TSP1‐Tg)‐SMC, constitutively overexpressing TSP‐1 in arterial SMC, compared to WT‐SMC suggesting specificity of Cr’s effect for TSP‐1. Together, our data reveal anti‐atherogenic effect of Cr on VSMC function and suggest TSP‐1 as a potential therapeutic target of Cr in diabetic vascular complications.