IMR Press / FBL / Volume 20 / Issue 4 / DOI: 10.2741/4337

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Chronic kidney disease alters vascular smooth muscle cell phenotype
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1 Center for Metabolic Disease Research, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
2 Cardiovascular Research Center, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
3 Division of Vascular Surgery, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
4 Department of Pathology and Laboratory Medicine, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
5 Section of Nephrology, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA 19140, USA
Academic Editor:Xiao-Feng Yang
Front. Biosci. (Landmark Ed) 2015, 20(4), 784–795; https://doi.org/10.2741/4337
Published: 1 January 2015
(This article belongs to the Special Issue Amylin in vasodilation, energy expenditure and inflammation)
Abstract

Vascular access dysfunction associated with arteriovenous grafts and fistulas contributes to the morbidity and mortality of chronic kidney disease (CKD) patients receiving hemodialysis. We hypothesized that the uremic conditions associated with CKD promote a pathophysiological vascular smooth muscle cell (VSMC) phenotype that contributes to neointimal hyperplasia. We analyzed the effect of culturing human VSMC with uremic serum. Expression of VSMC contractile marker genes was reduced 50-80% in cells exposed to uremic serum and the decreased expression was accompanied by changes in histone marks. There was an increase in proliferation in cells exposed to uremic conditions, with no change in the levels of apoptosis. Interestingly, we found that uremic serum inhibited PDGF-induced migration of VSMC. Histomorphometric analysis revealed venous neointimal hyperplasia in veins from chronic kidney disease (CKD) patients prior to any surgical manipulation as compared to veins from patients with no kidney disease. We conclude that uremia associated with CKD alters VSMC phenotype in vitro and contributes to neointimal hyperplasia formation in vivo contributing to the pathogenesis of vascular access dysfunction in CKD patients.

Keywords
Vascular Smooth Muscle Cells
Chronic Kidney Disease
Uremia
Hyperplasia
Vascular Access Dysfunction
Arteriovenous Fistula
Arteriovenous Grafts
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