The high glucose and 12(S)-hydroxyeicosatetraenoic acid (HETE) could alter vascular endothelial (VE)-cadherin and β‐catenin phosphorylation levels, but did not alter total protein expression. However, the 12/15-LO inhibitor, Cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC), antagonized the effect of high glucose on protein phosphorylation to mitigate destruction of the endothelial cell barrier, and the mouse diabetes mellitus model further confirmed these conclusions[1].
In Vitro
High glucose or 12(S)-HETE remarkably increased transendothelial dextran transport, and in combination it was increased further. Addition of the 12/15-LO inhibitor, CDC, partially suppressed dextran transport[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Wang X, et al. 12(S)-hydroxyeicosatetraenoic acid impairs vascular endothelial permeability by altering adherens junction phosphorylation levels and affecting the binding and dissociation of its components in high glucose-induced vascular injury. J Diabetes Investig. 2019;10(3):639-649.
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