Why the study?
Does AGE-modified BSA disrupt the VE-cadherin complex in cultured human and murine endothelial cells?
Does AGE-modified BSA disrupt the VE-cadherin complex in cultured human and murine endothelial cells?
Advanced glycation end-products disrupt the VE-cadherin complex in endothelial cells, increasing vascular permeability and migration, which may mechanistically contribute to diabetes- and aging-associated vascular complications.
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Hypothesis-generating for AGE-driven endothelial leak in diabetes; leaves open in vivo confirmation and clinical translation.
Otero et al. (2001) studied this question.
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