a pedf-derived peptide inhibits retinal neovascularization and blocks mobilization of bone marrow-derived endothelial progenitor cellspedf-derived肽抑制视网膜新生血管形成和块骨骨髓来源的内皮祖细胞的动员.pdfVIP
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a pedf-derived peptide inhibits retinal neovascularization and blocks mobilization of bone marrow-derived endothelial progenitor cellspedf-derived肽抑制视网膜新生血管形成和块骨骨髓来源的内皮祖细胞的动员
Hindawi Publishing Corporation
Experimental Diabetes Research
Volume 2012, Article ID 518426, 11 pages
doi:10.1155/2012/518426
Research Article
A PEDF-Derived Peptide Inhibits Retinal
Neovascularization and Blocks Mobilization of Bone
Marrow-Derived Endothelial Progenitor Cells
Richard Longeras,1 Krysten Farjo,1 Michael Ihnat,2 and Jian-Xing Ma1
1 Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma, OK 73104, USA
2 Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma, OK 73104, USA
Correspondence should be addressed to Jian-Xing Ma, jian-xing-ma@ouhsc.edu
Received 1 April 2011; Accepted 27 April 2011
Academic Editor: Gian Paolo Fadini
Copyright © 2012 Richard Longeras et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Proliferative diabetic retinopathy is characterized by pathological retinal neovascularization, mediated by both angiogenesis
(involving mature endothelial cells) and vasculogenesis (involving bone marrow-derived circulating endothelial progenitor
cells (EPCs)). Pigment epithelium-derived factor (PEDF) contains an N-terminal 34-amino acid peptide (PEDF-34) that has
antiangiogenic properties. Herein, we present a novel finding that PEDF-34 also possesses antivasculogenic activity. In the oxygen-
induced retinopathy (OIR) model using transgenic mice that have Tie2 promoter-driven GFP expression, we quantified Tie2GFP+
cells in bone marrow and peripheral blood by fluorescence-activated cell sorting (FACS). OIR significantly increased the number
of circulating Tie2-GFP+ at P16, correlating with the
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