Hyperglycaemia promotes cerebral barrier dysfunction through activation of protein kinase C-β-Reference-Cited by-同舟云学术

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Hyperglycaemia promotes cerebral barrier dysfunction through activation of protein kinase C-β

Published:2013-05-21 Issue:11 Volume:15 Page:993-999
ISSN:1462-8902
Container-title:Diabetes, Obesity and Metabolism
language:en
Short-container-title:Diabetes Obes Metab

Author:

Shao B.¹,Bayraktutan U.¹

Affiliation:

1. Division of Stroke Medicine, School of Clinical Sciences; The University of Nottingham; Nottingham; UK

Publisher

Wiley

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism,Internal Medicine

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1111/dom.12120/fullpdf

Reference33 articles.

1. Endothelial cell-cell junctions: happy together;Dejana;Nat Rev Mol Cell Biol,2004

2. A single gene product, claudin-1 or −2, reconstitutes tight junction strands and recruits occludin in fibroblasts;Furuse;J Cell Biol,1998

3. The influence of diabetes mellitus and hyperglycaemia on stroke incidence and outcome;Baird;J Clin Neurosci,2002

4. Free radicals, diabetes and endothelial dysfunction;Bayraktutan;Diabetes Obes Metab,2002

5. Preferential elevation of protein kinase C isoform beta II and diacylglycerol levels in the aorta and heart of diabetic rats: differential reversibility to glycemic control by islet cell transplantation;Inoguchi;Proc Natl Acad Sci USA,1992

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