April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
The relationships between endothelial progenitor cells, inflammation, and diabetic retinopathy.
Author Affiliations & Notes
  • Dawn A Sim
    NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust, London, United Kingdom
    Cell Biology, UCL Institute of Ophthalmology, London, United Kingdom
  • Pearse Andrew Keane
    NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust, London, United Kingdom
    Cell Biology, UCL Institute of Ophthalmology, London, United Kingdom
  • Catherine A Egan
    NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust, London, United Kingdom
  • Adnan Tufail
    NIHR Biomedical Research Centre, Moorfields Eye Hospital NHS Foundation Trust, London, United Kingdom
    Cell Biology, UCL Institute of Ophthalmology, London, United Kingdom
  • Marcus Fruttiger
    Cell Biology, UCL Institute of Ophthalmology, London, United Kingdom
  • Footnotes
    Commercial Relationships Dawn Sim, Allergan (F); Pearse Keane, Allergan (F); Catherine Egan, None; Adnan Tufail, Allergan (F), Novartis (F); Marcus Fruttiger, Amaken (F), AstraZeneca (F), Novartis (F)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 4003. doi:
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      Dawn A Sim, Pearse Andrew Keane, Catherine A Egan, Adnan Tufail, Marcus Fruttiger; The relationships between endothelial progenitor cells, inflammation, and diabetic retinopathy.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4003.

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

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Abstract

Purpose: To assess the relationship between endothelial progenitor cells, inflammation, and retinopathy phenotype in type 2 diabetes.

Methods: 26 patients with type 2 diabetes and 30 healthy controls were included. Patients were classified according to retinopathy grade. Mononuclear cells were isolated from peripheral blood, and endothelial progenitor cells (EPCs) identified by flow cytometry. Monocyte profiles were also assessed.

Results: The proportion of CD34+ EPCs co-expressing VEGFR2 was significantly greater in diabetes (5.77%±2.15) compared to healthy controls (2.14±2.00) (p=0.001). In diabetes, low levels of circulating CD34+ EPCs were also associated with monocytes co-expressing the monocyte activation marker CD163, and pro-angiogenic VEGFR2 (r=-0.53, p=0.04). On examination of monocyte subtypes- (1) pro-inflammatory monocytes (CD14+ CD16++) had a higher expression of CD163 (p=0.03) in patients with a body mass index of >30; (2) classical monocytes (CD14+ CD16-) had a higher expression of VEGFR2 and CD163 (p=0.03) in macular oedema; and (3) Intermediate monocytes (CD14+ CD16+) had a higher expression of VEGFR2 (p=0.05) in macular ischaemia.

Conclusions: Evaluation of cellular participants of vascular repair and chronic inflammation may offer an explanation as to why different phenotypes of diabetic retinopathy manifest, provide new insights into mechanisms of visual loss, and provide potential avenues for novel therapeutic approaches in this disease.

Keywords: 499 diabetic retinopathy • 557 inflammation • 529 flow cytometry  
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