Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 20, Issue -, Pages 784-795Publisher
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/4337
Keywords
Vascular Smooth Muscle Cells; Chronic Kidney Disease; Uremia; Hyperplasia; Vascular Access Dysfunction; Arteriovenous Fistula; Arteriovenous Grafts
Categories
Funding
- Temple University
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL108910, R01HL077288, R01HL110764, R01HL117654, R01HL094451] Funding Source: NIH RePORTER
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available