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Expression of cyclo-oxygenase-2 and downstream enzymes in diabetic fibrovascular epiretinal membranes
  1. A M Abu El-Asrar1,
  2. L Missotten2,
  3. K Geboes3
  1. 1
    Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia
  2. 2
    Department of Ophthalmology, University of Leuven, Leuven, Belgium
  3. 3
    Laboratory of Histochemistry and Cytochemistry, University of Leuven, Leuven, Belgium
  1. Professor A M Abu El-Asrar, Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, PO Box 245, Riyadh 11411, Saudi Arabia; abuasrar{at}ksu.edu.sa

Abstract

Background/aims: The inducible enzyme cyclo-oxygense-2 (COX-2) and its metabolic products are important mediators for angiogenesis. We investigated the expression of COX-2 and its downstream enzymes microsomal prostaglandin-E synthase (mPGES)-1, cytosolic PGES (cPGES) and thromboxane synthase (TXS), and correlated it with vascular endothelial growth factor (VEGF) expression and level of vascularisation in proliferative diabetic retinopathy (PDR) epiretinal membranes.

Methods: Membranes from five patients with active PDR and nine patients with inactive PDR were studied by immunohistochemistry.

Results: Vascular endothelial cells expressed COX-2, mPGES-1 and VEGF in 11, nine and six membranes, respectively. TXS was expressed in stromal cells in 12 membranes. There was no immunoreactivity for cPGES. There were significant correlations between number of blood vessels expressing CD34 and number of blood vessels expressing COX-2 (rs = 0.858; p<0.001), mPGES-1 (rs = 0.743; p = 0.002) and VEGF (rs = 0.845; p = 0.001) and number of cells expressing TXS (rs = 0.74; p = 0.002). The number of blood vessels expressing CD34 (p = 0.007), COX-2 (p = 0.027) and VEGF (p = 0.008) and stromal cells expressing mPGES-1 (p = 0.003), TXS (p = 0.04) and VEGF (p = 0.017) were significantly higher in active membranes than in inactive membranes.

Conclusion: COX-2 and its metabolic products might contribute to PDR angiogenesis.

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Footnotes

  • Funding: This work was supported by the College of Medicine Research Center, King Saud University Nasser Al Rasheed Fund.

  • Competing interests: None.

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