323 The Role of Endothelial Progenitor Cells in Neovascularization of Ischemic Retina Through Sdf-1/Cxcr4 Axis in Oxygen-Induced Retinopathy Rat Model
Retinopathy of prematurity (ROP) is a common cause of blindness in preterm infants worldwide, despite laser treatment. Animal models of oxygeninduced retinopathy (OIR) have been developed to investigate physiological events that lead to the occurrence of this disease. It is known that endothelial pr...
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Published in | Pediatric research Vol. 68; no. Suppl 1; p. 166 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Nature Publishing Group US
01.11.2010
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Subjects | |
Online Access | Get full text |
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Summary: | Retinopathy of prematurity (ROP) is a common cause of blindness in preterm infants worldwide, despite laser treatment. Animal models of oxygeninduced retinopathy (OIR) have been developed to investigate physiological events that lead to the occurrence of this disease. It is known that endothelial progenitor cells (EPCs), derived from bone-marrow, are involved in vascular repair and neovascularization. In the present study we investigate the retinal expression of the SDF-1/ CXCR4 axis, its role in the recruitment of EPCs to the hypoxic retina, and the relationship between these cells and the development of neovascularization in a 50/10 OIR rat model. Our results show increased production of SDF-1 by endothelial cells and neurons in OIR retinas, and enhanced expression of CXCR4 mainly in Müller cells. We have also found in peripheral blood of OIR rats a decreased number of colony-forming units of EPCs. Whether this is due to the presence of functionally impaired EPCs or to the inability of an exhausted bone-marrow to produce enough progenitor cells to cope with the high demands of the process of retinal neovacularization, remains unanswered. We demonstrate in this study that SDF-1/CXCR4 axis, EPCs dysfunction and probably Müller cells, are involved in retinal neovascularization in a 50/10 rat model of OIR. These results warrant further studies. |
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ISSN: | 0031-3998 1530-0447 |
DOI: | 10.1203/00006450-201011001-00323 |