June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Endothelial Progenitor Cells in Bone Marrow, Blood, and Retina Respond Dynamically to Murine Oxygen-Induced Retinopathy
Author Affiliations & Notes
  • Bliss O'Bryhim
    Ophthalmology, University of Kansas Medical Center, Kansas City, KS
    Molecular & Integrative Physiology, Univ of Kansas Medical Center, Kansas City, KS
  • R. Sid White
    Ophthalmology, University of Kansas Medical Center, Kansas City, KS
  • Robert Symons
    Ophthalmology, University of Kansas Medical Center, Kansas City, KS
    Department of Surgery, University of Melbourne, Melbourne, VIC, Australia
  • Footnotes
    Commercial Relationships Bliss O'Bryhim, None; R. Sid White, None; Robert Symons, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 4536. doi:
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      Bliss O'Bryhim, R. Sid White, Robert Symons; Endothelial Progenitor Cells in Bone Marrow, Blood, and Retina Respond Dynamically to Murine Oxygen-Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4536.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Purpose
 

Bone marrow-derived endothelial progenitor cells (EPCs) have been shown to contribute to angiogenesis in a variety of pathologies, including metastatic disease, wound healing, and diabetic vascular disorders. Recent work has indicated that EPCs additionally play an important role in both retinopathy of prematurity (ROP) and in the murine model of ROP, oxygen-induced retinopathy (OIR). The purpose of this study is to characterize response of this cell population to OIR during vaso-obliteration and revascularization.

 
Methods
 

C57BL/6J pups were exposed to 75% oxygen for 120 hours beginning on post-natal day 7 (P7). Mice were sacrificed at daily time points from P7 to P13, and also at P7.5 and P9.5. Live, CD45-/CD34+/CD133+ EPCs were enumerated in bone marrow and blood samples using flow cytometry and expressed as a fraction of all live/CD45- cells. Left retinas were stained for the presence of CD34+/CD133+ EPCs and were counted by an observer blinded to date. Corresponding right retinas were stained with isolectin B4, and the avascular area was measured using ImageJ software.

 
Results
 

The number of CD34+/CD133+ cells in the bone marrow decreased initially in response to hyperoxia from P7 to P8, with a peak increase on P9 (0.817%) followed by a gradual decline to 0.270% on P13 (Figure). Circulating CD34+/CD133+ cells increased early in OIR but declined ten-fold from P8 (0.310%) to P10 (0.030%), after which the number increased through P12. The number of CD34+/CD133+ cells recruited to the retina mirrored patterns of circulating cells, with 2 peaks of recruitment on P7.5 (53.7cells/mm2) and P11 (40.3cells/mm2). Retinal avascular areas increased ten-fold from P7 to a maximum on P11 (5.14mm2), and began to decrease by P12.

 
Conclusions
 

Bone marrow-derived EPCs are a dynamic population of cells that respond to tissue injury caused by extended hyperoxic stress. Further studies are needed to clarify if the influx of EPCs into the retina on P11 is directly responsible for reduction in avascular area between P11 and P12. A better understanding of their recruitment from the bone marrow to the retina where they contribute to vascular repair may serve to improve therapies available for vasoproliferative retinopathies, including ROP.

 
 
Figure. Quantification of CD34+/CD133+ cells in bone marrow, blood, and retina, and retinal avascular area during the oxygen-induced retinopathy model.
 
Figure. Quantification of CD34+/CD133+ cells in bone marrow, blood, and retina, and retinal avascular area during the oxygen-induced retinopathy model.
 
Keywords: 706 retinopathy of prematurity • 687 regeneration • 688 retina  
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