Chronic kidney disease alters vascular smooth muscle cell phenotype

M. Alexandra Monroy, Jianhua Fang, Shan Li, Lucas Ferrer, Mark P. Birkenbach, Iris J. Lee, Hong Wang, Xiao Feng Yang, Eric T. Choi

Research output: Contribution to journalArticlepeer-review

58 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)784-795
Number of pages12
JournalFrontiers in Bioscience - Landmark
Issue number4
StatePublished - Jan 15 2015

Bibliographical note

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© 2015, Frontiers in Bioscience. All rights reserved.


  • Arteriovenous fistula
  • Arteriovenous grafts
  • Chronic kidney disease
  • Hyperplasia
  • Uremia
  • Vascular access dysfunction
  • Vascular smooth muscle cells


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