Source:http://linkedlifedata.com/resource/pubmed/id/16699065
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2006-7-14
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| pubmed:abstractText |
Vascular endothelial cells (ECs), which regulate vascular tonus, serve as a barrier at the interface of vascular tissue. It is generally believed that alteration of this barrier is correlated with diabetic complications; however, a detailed mechanism has not been elucidated. This study examined alteration of bovine arterial EC functions stimulated by a thromboxane A2 analog (9,11-dideoxy-11 alpha,9 alpha-epoxymethano prostaglandin F(2 alpha); U46619) under normal and high-glucose (HG) conditions. U46619 treatment increased EC layer permeability in a time- and dose-dependent fashion. This response initially disrupted calcium-dependent EC-to-EC connections, namely, vascular endothelial cadherin (VE-CaD). Thereafter, EC force development in association with morphological changes was detected employing a reconstituted EC fiber technique, resulting in paracellular hole formation in the EC layer. Thus, we confirmed that U46619-induced enhancement of EC layer permeability involves these sequential steps. Similar trials were performed using a concentration twice that of normal glucose (22.2 mM glucose for 48 h). This treatment significantly enhanced U46619-induced EC layer permeability; furthermore, increases in both rate of VE-CaD disruption and EC fiber contraction were evident. Inhibition of calcium-independent protein kinase C and diacylglycerol kinase indicated that the glucose-dependent increase in VE-CaD disruption was mediated by a calcium-independent mechanism. Moreover, EC contraction was regulated by a typical calcium-independent pathway associated with rho kinase and actin stress fiber. Contraction was also enhanced under HG conditions. This investigation revealed that glucose-dependent enhancement of EC layer permeability is related to increases in VE-CaD disruption and EC contraction. Increases in both parameters were mediated by alteration of a calcium-independent pathway.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1,2-bis(2-aminophenoxy)ethane-N,N,N'...,
http://linkedlifedata.com/resource/pubmed/chemical/15-Hydroxy-11 alpha,9...,
http://linkedlifedata.com/resource/pubmed/chemical/Acetophenones,
http://linkedlifedata.com/resource/pubmed/chemical/Benzopyrans,
http://linkedlifedata.com/resource/pubmed/chemical/Benzoquinones,
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents,
http://linkedlifedata.com/resource/pubmed/chemical/rottlerin,
http://linkedlifedata.com/resource/pubmed/chemical/stemphone
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
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| pubmed:issn |
0022-3565
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
318
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
530-9
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16699065-15-Hydroxy-11 alpha,9...,
pubmed-meshheading:16699065-Acetophenones,
pubmed-meshheading:16699065-Animals,
pubmed-meshheading:16699065-Benzopyrans,
pubmed-meshheading:16699065-Benzoquinones,
pubmed-meshheading:16699065-Cadherins,
pubmed-meshheading:16699065-Calcium,
pubmed-meshheading:16699065-Capillary Permeability,
pubmed-meshheading:16699065-Cattle,
pubmed-meshheading:16699065-Cell Communication,
pubmed-meshheading:16699065-Cells, Cultured,
pubmed-meshheading:16699065-Egtazic Acid,
pubmed-meshheading:16699065-Endothelial Cells,
pubmed-meshheading:16699065-Enzyme Inhibitors,
pubmed-meshheading:16699065-Extracellular Space,
pubmed-meshheading:16699065-Glucose,
pubmed-meshheading:16699065-Image Processing, Computer-Assisted,
pubmed-meshheading:16699065-Immunohistochemistry,
pubmed-meshheading:16699065-Isometric Contraction,
pubmed-meshheading:16699065-Muscle, Smooth, Vascular,
pubmed-meshheading:16699065-Muscle Contraction,
pubmed-meshheading:16699065-Vasoconstrictor Agents
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| pubmed:year |
2006
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| pubmed:articleTitle |
High-glucose-altered endothelial cell function involves both disruption of cell-to-cell connection and enhancement of force development.
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| pubmed:affiliation |
Department of Pharmacology, School of Pharmaceutical Sciences, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-0555, Japan. kojinobe@pharm.showa-u.ac.jp
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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