Uremia induces functional incompetence of bone marrow-derived stromal cells
- Authors
- Noh, Hyunjin; Yu, Mi Ra; Kim, Hyun Joo; Jeon, Jin Seok; Kwon, Soon Hyo; Jin, So Young; Lee, Jeeyun; Jang, Jiryeon; Park, Joon Oh; Ziyadeh, Fuad; Han, Dong Cheol; Lee, Hi Bahl
- Issue Date
- Jan-2012
- Publisher
- Oxford University Press
- Keywords
- angiogenesis; bone marrow-derived stromal cells; cardiovascular disease; chronic kidney disease
- Citation
- Nephrology Dialysis Transplantation, v.27, no.1, pp 218 - 225
- Pages
- 8
- Journal Title
- Nephrology Dialysis Transplantation
- Volume
- 27
- Number
- 1
- Start Page
- 218
- End Page
- 225
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/15450
- DOI
- 10.1093/ndt/gfr267
- ISSN
- 0931-0509
1460-2385
- Abstract
- Background. Chronic kidney disease (CKD) is associated with increased risk for cardiovascular diseases (CVD). We hypothesized that inadequate angiogenic response in uremic patients could result from dysfunction of bone marrow-derived stromal cells [mesenchymal stem cells (MSCs)]. Methods. We investigated whether MSCs are functionally competent in uremia induced by partial kidney ablation in C57Bl/6J mice. Results. Uremic MSCs showed decreased expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR) 1 and stromal cell-derived factor (SDF)-1 alpha, increased cellular senescence, decreased proliferation, defects in migration in response to VEGF and SDF-1 alpha and in vitro tube formation. Interestingly, the expression of fibroblast-specific protein-1 was higher in uremic MSCs. Uremia decreased hypoxia-inducible factor-1 alpha, VEGF and VEGFR1 expression under hypoxia and Akt phosphorylation in both basal and VEGF-stimulated states. A diminished mitogenic effect on endothelial proliferation was observed in conditioned media from uremic MSCs. In addition, intravital microscopic analysis showed decreased angiogenesis in uremic MSCs. Conclusion. These results clearly demonstrate the functional incompetence in MSCs under uremic conditions and may significantly contribute to the disproportionately high risk for CVD in patients with CKD.
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Collections - College of Medicine > Department of Pathology > 1. Journal Articles
- College of Medicine > Department of Internal Medicine > 1. Journal Articles
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