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A.-F. Li, S.-M. Lee, P.-H. Yin, C.-W. Chi; Dexamethasone (Dex) Ameliorates Reduced VE-Cadherin Expression by High Glucose in Microvascular Endothelial cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4901.
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To determine whether endothelial barrier associated molecule-VE-Cadherin plays a role in the mechanism of diabetic macular edema, the expression of VE-Cadherin was measured under high glucose condition or Dex treatment.
Western blot analysis was performed to determine VE-Cadherin expression in Rat microvascular endothelial cells (RMECs) grown in normal glucose (5mM) medium, high glucose(25mM) medium for 7 days, high glucose medium with dexamethasone (Dex) 50, 100, or 500nM for 48h. RT-PCR analysis was done in parallel.
Western blot analysis showed decreased VE-Cadherin in cells grown in high glucose condition (59.3±19% of control, p=0.002, n=5) compared to cells in normal medium. With the treatment of dexamethasone in high glucose medium, reduced VE-Cadherin returned to be comparable with cells in normal medium, significantly increased than cells in high glucose medium only (98.21±22% of control p=0.02, n=5, in Dex 50nM; 104.4±12% of control p=0.04, n=5, in 100nM Dex). No change of VE-Cadherin mRNA has been shown in cells treated with Dex.
Dexamethasone resulted in changes of VE-cadherin in endothelial cells in high glucose condition. This might be part of the mechanism for intravitreal injection of corticosteroid such as triamcinolone acetonide to reduce diabetic macular edema.
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