To show that your sera induce an increase in endothelial cell permeability you should measure this directly first by showing a reduction in transendothelial resistance across the monolayer and/or increases in movement of a dye (FITC-dextran) across the monolayer. Once you confirm that these is increased permeability, then you should look at the mechanisms involved. You could measure cellular levels of VE cadherin and other junctional markers. It is also possibly that the sera that you are testing may cause injury to the endothelial cells which can be measured using assays to quantify cell death or injury (e.g. release of lactate dehydrogenase) assays.

To show that your sera induce an increase in endothelial cell permeability you should measure this directly first by showing a reduction in transendothelial resistance across the monolayer and/or increases in movement of a dye (FITC-dextran) across the monolayer. Once you confirm that these is increased permeability, then you should look at the mechanisms involved. You could measure cellular levels of VE cadherin and other junctional markers. It is also possibly that the sera that you are testing may cause injury to the endothelial cells which can be measured using assays to quantify cell death or injury (e.g. release of lactate dehydrogenase) assays.

I agree with Caroline that permeability should be measured using transendothelial resistance or leakage of a dye through to a monolayer of confluent endothelial cells. I would be hesitant to claim you investigated permeability if expression is the only thing you measured. It is also becoming more common to measure permeability in vivo as well if that is an option or if there is an animal model you can use.

VE-cadherin is typically associated with Adherens junctions. Occludin and ZO-1 are more for tight junctions. These junction proteins are very closely linked in function and protein assembly. Hence why when one is disrupted, it can have a significant effect on the other. I would definitely look at the distribution of the protein as well as expression.

Endothelial permeability change can be directly measured by the xCelligence RTCA system. The expression of VE-Cadherin may not be the best choice of measuring the monolayer resistance, as dynamic changes of resistance often happen without reducing VE-Cadherin surface expression levels. If you choose to use imaging to quantitatively measure the permeability, you could measure the area of the intercellular space between neighbouring cells induced by sera from Dengue infected patients or normal controls. This could be achieved by staining VE-Cadherin and delineating the cell border using FIJI or other softwares.

I agree with Caroline as endothelial cell permeability should be measured by transendothelial resistance / FITC-dextran method along with VE Cadherin and ZO1 expression.