June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Influence of Proliferative Diabetic Retinopathy Aqueous in Causing Defective CD34 cells
Author Affiliations & Notes
  • Sankarathi Balaiya
    Ophthalmology, Univ of Florida College of Med, Jacksonville, FL
  • Maria Grant
    Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, FL
  • K V Chalam
    Ophthalmology, Univ of Florida College of Med, Jacksonville, FL
  • Footnotes
    Commercial Relationships Sankarathi Balaiya, None; Maria Grant, None; K V Chalam, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 274. doi:
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      Sankarathi Balaiya, Maria Grant, K V Chalam; Influence of Proliferative Diabetic Retinopathy Aqueous in Causing Defective CD34 cells. Invest. Ophthalmol. Vis. Sci. 2013;54(15):274.

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

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Purpose: Proliferative diabetic retinopathy (PDR), a major complication of diabetes induces retinal microvascular endothelial dysfunction lead to decreased retinal perfusion, hypoxia and subsequent induction of angiogenic factors. Endothelial progenitor cells, a subpopulation of the circulating mononuclear cells are recruited to sites requiring vascular repair and can contribute to the repair and viability of the vasculature. However, in diabetes, dysfunctional EPCs may not repair this injury and promote development of acellular capillaries and sustained retinal ischemia. In this study, we investigated whether angiogenic cytokines present in aqueous of PDR subjects might affect the reparative nature of CD34 cells.

Methods: Aqueous fluid was obtained from individuals with PDR undergoing pars plana vitrectomies in accordance with Institutional review board at the University of Florida, Jacksonville. Aqueous fluid from healthy individuals who underwent cataract extraction without any ocular diseases served as controls. Mobilized healthy human CD34 cells were maintained in an undifferentiated state and treated with 1% and 5% concentration of PDR and control aqueous fluid. The effect of PDR aqueous on CD34 cells were analyzed using trypan blue exclusion assay on day 4 and day 7. In addition, migration chamber assay was performed on aqueous enriched CD34 cells (10,000 cells); conditioned medium was analyzed with nanoelectrospray ionization mass spectrometry (nESI-MS).

Results: In presence of aqueous, CD34 cells showed increased proliferation in a time-dependent manner. On day 4, they did not showed increased proliferation compared to control (12.8x106 Vs 20x106), whereas proliferation increased on day 7 (3.73x106 Vs 3.06x106). Pretreated CD34 cells with varying concentration of aqueous fluid from PDR patients did not cause any increase in migratory response compared to aqueous fluid from healthy patients. However, the migratory response was significantly reduced to 12.2% in comparison to control after treatment with 5% concentration of aqueous fluid from PDR patients (p<0.05).

Conclusions: Our study results suggests that the proteins/cytokines that are secreted and released into the aqueous due to diseased condition (PDR) severely impairs the reparative nature of endothelial progenitor cells.

Keywords: 499 diabetic retinopathy • 721 stem cells • 490 cytokines/chemokines  

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