The effect of hyperglycaemia on permeability and tight junction components in human retinal and choroidal endothelial cells

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Diabetic retinopathy is the leading cause of preventable blindness in the working population. The main cause of visual loss in diabetic retinopathy is diabetic macular oedema caused by an increase in microvascular endothelial permeability. The aim of this project was to determine the effect of hyperglycaemia, in vitro, on human choroidal (hCEC) and retinal microvascular endothelial cells (hREC).


Microvascular permeability was assessed through passage of dye through a confluent cell layer in the presence of hyperglycaemia. Microarray analysis and western blotting was used to compare the expression of selected tight junction molecules (Occludin, Claudin-5, JAM-A and JAM-C) and adheren junction (VE-Cadherin) molecules was compared between hCEC and hREC and with hyperglycaemia.


Hyperglycaemic conditions significantly increased the permeability in both hCEC and hREC. Microarray analysis and western blotting determined that the baseline hREC expression of occludin and claudin-5 was higher than hCEC. In hREC exposed to hyperglycaemia claudin-5, occludin and JAM-A were found to be reduced. None of the proteins were decreased by hyperglycaemia in hCEC.


Although hyperglycaemia increased permeability in both hCEC and hREC, tight junction protein expression was only reduced in hREC, indicating a different mechanism of increased permeability in hCEC compared to hREC.


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