Proteolytic Degradation of VE-Cadherin Alters the Blood-Retinal Barrier in Diabetes
Open Access
- 1 September 2007
- journal article
- Published by American Diabetes Association in Diabetes
- Vol. 56 (9), 2380-2387
- https://doi.org/10.2337/db06-1694
Abstract
OBJECTIVE— Increased vascular permeability due to alteration of the blood-retinal barrier (BRB) is one of the major complications in early diabetes. The aim of the present study was to determine whether diabetes alters the cellular expression and distribution of the adherens junction protein vascular endothelial (VE)-cadherin in retinal endothelial cells and if this alteration is mediated by proteinase activity.Keywords
This publication has 41 references indexed in Scilit:
- VEGF controls endothelial-cell permeability by promoting the β-arrestin-dependent endocytosis of VE-cadherinNature, 2006
- Ischemia-induced cleavage of cadherins in NRK cells requires MT1-MMP (MMP-14)American Journal of Physiology-Renal Physiology, 2006
- Ischemia-induced cleavage of cadherins in NRK cells: evidence for a role of metalloproteinasesAmerican Journal of Physiology-Renal Physiology, 2005
- VE-cadherin is not required for the formation of nascent blood vessels but acts to prevent their disassemblyBlood, 2005
- Protein GlycationCirculation Research, 2004
- Regulation of matrix biology by matrix metalloproteinasesCurrent Opinion in Cell Biology, 2004
- VE-cadherin-p120 interaction is required for maintenance of endothelial barrier functionAmerican Journal of Physiology-Lung Cellular and Molecular Physiology, 2004
- The tight junction: a multifunctional complexAmerican Journal of Physiology-Cell Physiology, 2004
- VE-cadherin: adhesion at arm's lengthAmerican Journal of Physiology-Cell Physiology, 2004
- Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT MethodMethods, 2001