Nitric Oxide Cytoskeletal–Induced Alterations Reverse the Endothelial Progenitor Cell Migratory Defect Associated With Diabetes-Reference-Cited by-同舟云学术

Nitric Oxide Cytoskeletal–Induced Alterations Reverse the Endothelial Progenitor Cell Migratory Defect Associated With Diabetes

Published:2006-01-01 Issue:1 Volume:55 Page:102-109
ISSN:0012-1797
Container-title:Diabetes
language:en
Short-container-title:

Author:

Segal Mark S.¹,Shah Ronak¹,Afzal Aqeela²,Perrault Cecile M.³,Chang Kyunghee²,Schuler Anna¹,Beem Elaine¹,Shaw Lynn C.²,Li Calzi Sergio²,Harrison Jeffrey K.²,Tran-Son-Tay Roger³⁴,Grant Maria B.²

Affiliation:

1. Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida

2. Division of Pharmacology and Therapeutics, University of Florida, Gainesville, Florida

3. Department of Biomedical Engineering, University of Florida, Gainesville, Florida

4. Department of Mechanical and Aerospace Engineering, University of Florida, Gainesville, Florida

Abstract

Stromal-derived factor-1 (SDF-1) is a critical chemokine for endothelial progenitor cell (EPC) recruitment to areas of ischemia, allowing these cells to participate in compensatory angiogenesis. The SDF-1 receptor, CXCR4, is expressed in developing blood vessels as well as on CD34+ EPCs. We describe that picomolar and nanomolar concentrations of SDF-1 differentially influence neovascularization, inducing CD34+ cell migration and EPC tube formation. CD34+ cells isolated from diabetic patients demonstrate a marked defect in migration to SDF-1. This defect is associated, in some but not all patients, with a cell surface activity of CD26/dipeptidyl peptidase IV, an enzyme that inactivates SDF-1. Diabetic CD34+ cells also do not migrate in response to vascular endothelial growth factor and are structurally rigid. However, incubating CD34+ cells with a nitric oxide (NO) donor corrects this migration defect and corrects the cell deformability. In addition, exogenous NO alters vasodilator-stimulated phosphoprotein and mammalian-enabled distribution in EPCs. These data support a common downstream cytoskeletal alteration in diabetic CD34+ cells that is independent of growth factor receptor activation and is correctable with exogenous NO. This inability of diabetic EPCs to respond to SDF-1 may contribute to aberrant tissue vascularization and endothelial repair in diabetic patients.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

Link

https://journals.org/diabetes/diabetes/article-pdf/55/1/102/382574/zdb00106000102.pdf

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