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Uric acid-induced endothelial dysfunction is associated with mitochondrial alterations and decreased intracellular ATP concentrations

Title
Uric acid-induced endothelial dysfunction is associated with mitochondrial alterations and decreased intracellular ATP concentrations
Authors
Sanchez-Lozada L.G.Lanaspa M.A.Cristobal-Garcia M.Garcia-Arroyo F.Soto V.Cruz-Robles D.Nakagawa T.Yu M.A.Kang D.-H.Johnson R.J.
Ewha Authors
강덕희
SCOPUS Author ID
강덕희scopus
Issue Date
2013
Journal Title
Nephron - Experimental Nephrology
ISSN
1660-2129JCR Link
Citation
vol. 121, no. 41337, pp. e71 - e78
Indexed
SCOPUS WOS scopus
Abstract
Background/Aims: Endothelial dysfunction is associated with mitochondrial alterations. We hypothesized that uric acid (UA), which can induce endothelial dysfunction in vitro and in vivo, might also alter mitochondrial function. Methods: Human aortic endothelial cells were exposed to soluble UA and measurements of oxidative stress, nitric oxide, mitochondrial density, ATP production, aconitase-2 and enoyl Co-A hydratase-1 expressions, and aconitase-2 activity in isolated mitochondria were determined. The effect of hyperuricemia induced by uricase inhibition in rats on renal mitochondrial integrity was also assessed. Results: UA-induced endothelial dysfunction was associated with reduced mitochondrial mass and ATP production. UA also decreased aconitase-2 activity and lowered enoyl CoA hydratase-1 expression. Hyperuricemic rats showed increased mitDNA damage in association with higher levels of intrarenal UA and oxidative stress. Conclusions: UA-induced endothelial dysfunction is associated with mitochondrial alterations and decreased intracellular ATP. These studies provide additional evidence for a deleterious effect of UA on vascular function that could be important in the pathogenesis of hypertension and vascular disease. © 2012 S. Karger AG, Basel.
DOI
10.1159/000345509
Appears in Collections:
의과대학 > 의학과 > Journal papers
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