April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Elevation of Vitreous Endocan Levels in Proliferative Diabetic Retinopathy
Author Affiliations & Notes
  • Ajay Shalwala
    Vanderbilt Eye Institute, Nashville, Tennessee
  • Philippe Lassalle
    Campus de l’Institut Pasteur de Lille, Lille, France
  • Nathalie De Freitas Caires
    Campus de l’Institut Pasteur de Lille, Lille, France
  • Maryse Delehedde
    Campus de l’Institut Pasteur de Lille, Lille, France
  • Kevin Wise
    Vanderbilt Eye Institute, Nashville, Tennessee
  • Hassanain Toma
    Vanderbilt Eye Institute, Nashville, Tennessee
  • Erin Fulchiero
    Vanderbilt Eye Institute, Nashville, Tennessee
  • Franco Recchia
    Vanderbilt Eye Institute, Nashville, Tennessee
  • Footnotes
    Commercial Relationships  Ajay Shalwala, None; Philippe Lassalle, INSERM (E), Lunginnov (C); Nathalie De Freitas Caires, Lunginnov (E); Maryse Delehedde, Lunginnov (E); Kevin Wise, None; Hassanain Toma, None; Erin Fulchiero, None; Franco Recchia, Alcon (C), Allergan (C)
  • Footnotes
    Support  NIH Grant EY008126, RPB Unrestricted Grant to Vanderbilt Ophthalmology
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1295. doi:
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      Ajay Shalwala, Philippe Lassalle, Nathalie De Freitas Caires, Maryse Delehedde, Kevin Wise, Hassanain Toma, Erin Fulchiero, Franco Recchia; Elevation of Vitreous Endocan Levels in Proliferative Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1295.

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

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Proliferative diabetic retinopathy (PDR) is an increasingly common cause of vision loss resulting from retinal neovascularization. Identification of retinal angiogenesis factors may lead to new anti-angiogenic therapy. We have demonstrated increased expression of esm1, the gene coding for endocan, in rodent models. This translational study was done to determine whether vitreous endocan levels are elevated in PDR patients to rationalize further study of endocan in PDR pathogenesis.


Undiluted vitreous and serum samples were obtained from diabetic and non-diabetic patients undergoing vitrectomy. The endocan levels in these samples were measured in duplicate by sandwich ELISA using two commercialized monoclonal antibodies against human endocan (Lunginnov, Lille, France). Concentrations were compared using the Wilcoxon two-sample test and one-way analysis of variance (ANOVA).


Samples from 62 patients (24 with PDR, 12 diabetics without treatment-requiring retinopathy, and 26 non-diabetics) were analyzed. Vitreous endocan concentrations were significantly different among the three groups (p=0.001 by ANOVA). PDR patients had a mean vitreous endocan level of 1.92 ng/mL, while non-diabetic patients had a mean of 0.78 ng/mL (p=0.004). Serum endocan concentrations did not differ significantly between the PDR (1.67 ng/mL) and non-diabetic (1.71 ng/mL) groups (p=0.72). Compared to non-diabetics, the vitreous-serum endocan concentration ratio was significantly higher in both PDR patients (1.4 ± 0.5 vs 0.5 ± 0.3 [95% CI], p=0.006) and in diabetics without PDR (1.2 ± 0.3 vs 0.5 ± 0.3 [95% CI], p=0.01).  


Vitreous endocan levels were elevated in PDR patients relative to non-diabetics. Serum endocan levels were similar, suggesting that endocan may be released locally by ischemic retina. The elevation of endocan levels in the vitreous of PDR patients suggests that endocan may play a role in PDR pathogenesis. Its mechanism of action and potential as a therapeutic target warrant further study.

Keywords: diabetic retinopathy • retinal neovascularization 

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