کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2048853 1074104 2010 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Advanced glycation end products increase endothelial permeability through the RAGE/Rho signaling pathway
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش گیاه شناسی
پیش نمایش صفحه اول مقاله
Advanced glycation end products increase endothelial permeability through the RAGE/Rho signaling pathway
چکیده انگلیسی

Although increased vascular permeability is known to be a major characteristic of diabetic vasculopathy, the precise mechanisms and relevance of advanced glycation end products (AGE) to hyperpermeability of vessels remains unclear. Here, we studied changes in cytoskeletal configuration and the signaling mechanism induced by AGE in human endothelial cells. AGE-BSA stimulation induced Rho activation, intercellular gap formation, prominent actin stress fiber and cell contraction without changing VE-cadherin, and subsequently transendothelial diffusion of FITC-labeled dextran. These processes induced by AGE-BSA were inhibited by either Rho-kinase inhibitor Y27632 or anti-RAGE antibody. We also showed that RhoA and RAGE spontaneously formed a complex. These findings suggest that activation of RAGE/Rho is involved in AGE-BSA-induced hyperpermeability through gap formation and actin reorganization in diabetes.Structured summaryMINT-7301170: Rhotekin (uniprotkb:Q9BST9) physically interacts (MI:0915) with RhoA (uniprotkb:P61586) by pull down (MI:0096)MINT-7301204, MINT-7301186: RhoA (uniprotkb:P61586) physically interacts (MI:0915) with RAGE (uniprotkb:Q15109) by anti bait coimmunoprecipitation (MI:0006)

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: FEBS Letters - Volume 584, Issue 1, 4 January 2010, Pages 61–66
نویسندگان
, , , , ,