Nitric Oxide Cytoskeletal–Induced Alterations Reverse the Endothelial Progenitor Cell Migratory Defect Associated With Diabetes
作者： M. S. Segal , R. Shah , A. Afzal , C. M. Perrault , K. Chang
DOI: 10.2337/DIABETES.55.01.06.DB05-0803
关键词:
摘要: Stromal-derived factor-1 (SDF-1) is a critical chemokine for endothelial progenitor cell (EPC) recruitment to areas of ischemia, allowing these cells participate in compensatory angiogenesis. The SDF-1 receptor, CXCR4, expressed developing blood vessels as well on CD34+ EPCs. We describe that picomolar and nanomolar concentrations differentially influence neovascularization, inducing migration EPC tube formation. isolated from diabetic patients demonstrate marked defect SDF-1. This associated, some but not all patients, with surface activity CD26/dipeptidyl peptidase IV, an enzyme inactivates Diabetic also do migrate response vascular growth factor are structurally rigid. However, incubating nitric oxide (NO) donor corrects this the deformability. In addition, exogenous NO alters vasodilator-stimulated phosphoprotein mammalian-enabled distribution These data support common downstream cytoskeletal alteration independent receptor activation correctable NO. inability EPCs respond may contribute aberrant tissue vascularization repair patients.
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