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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-3-29
pubmed:abstractText
The mechanisms underlying the hypoxia-induced disruption of the barrier function of neural vasculature were analyzed with reference to the expression of claudin-5, a component of tight junctions between neural endothelial cells. The movement of claudin-5 from the cytoplasm to the plasma membrane of cultured confluent brain-derived endothelial (bEND.3) cells was closely correlated with the increase in the transendothelial electrical resistance. Inhibition of the expression of claudin-5 by RNAi resulted in a reduction of transendothelial electrical resistance, indicating a critical role of claudin-5 in the barrier property. Hypoxia (1% O(2)) altered the location of claudin-5 in the plasma membrane and the level of claudin-5 protein in bEND.3 cells, and these changes were accompanied by a decrease in the transendothelial electrical resistance. In vivo the claudin-5 molecules were expressed under normoxia in the plasma membrane of retinal microvascular endothelial cells but were significantly reduced under hypoxic conditions. Tracer experiments revealed that the barrier function of hypoxic retinal vasculature with depressed claudin-5 expression was selectively disrupted against small molecules, which is very similar to the phenotype of claudin-5-deficient mice. These in vitro and in vivo data indicate that claudin-5 is a target molecule of hypoxia leading to the disruption of the barrier function of neural vasculature.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-10074486, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-10508865, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-11102513, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-11283726, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-11782481, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-11893586, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12475568, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12538770, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12714657, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12734665, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12743111, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12808449, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12902832, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-12907427, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-14505058, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-14567987, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-14702427, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-14755541, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-14996944, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15075229, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15174142, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15206924, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15207256, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15221411, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15316464, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15795901, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-15820555, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-16185289, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-16460278, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-16537104, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-16550326, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-1693235, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-1991159, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-338327, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-3543687, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-7250491, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-7544346, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-7903970, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-8022811, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-8276896, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-8736632, http://linkedlifedata.com/resource/pubmed/commentcorrection/17392177-9647647
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0002-9440
pubmed:author
pubmed:issnType
Print
pubmed:volume
170
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1389-97
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:17392177-Animals, pubmed-meshheading:17392177-Mice, pubmed-meshheading:17392177-Brain, pubmed-meshheading:17392177-Anoxia, pubmed-meshheading:17392177-Blood-Brain Barrier, pubmed-meshheading:17392177-Microscopy, Fluorescence, pubmed-meshheading:17392177-Male, pubmed-meshheading:17392177-Capillary Permeability, pubmed-meshheading:17392177-Membrane Proteins, pubmed-meshheading:17392177-Time Factors, pubmed-meshheading:17392177-Retinal Vessels, pubmed-meshheading:17392177-RNA, Messenger, pubmed-meshheading:17392177-Cell Line, pubmed-meshheading:17392177-Mice, Inbred C57BL, pubmed-meshheading:17392177-Cell Hypoxia, pubmed-meshheading:17392177-Electric Impedance, pubmed-meshheading:17392177-Transfection, pubmed-meshheading:17392177-Endothelial Cells, pubmed-meshheading:17392177-Gene Expression
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