| pubmed-article:18996441 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18996441 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:18996441 | lifeskim:mentions | umls-concept:C1154393 | lld:lifeskim |
| pubmed-article:18996441 | lifeskim:mentions | umls-concept:C0332453 | lld:lifeskim |
| pubmed-article:18996441 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
| pubmed-article:18996441 | lifeskim:mentions | umls-concept:C0813872 | lld:lifeskim |
| pubmed-article:18996441 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:18996441 | pubmed:dateCreated | 2008-12-16 | lld:pubmed |
| pubmed-article:18996441 | pubmed:abstractText | The aim of the present study was to examine the signaling pathways of hypoxia followed by reoxygenation (H/R)-induced disruption of the blood-brain-barrier (BBB) in a co-culture of astrocytes and brain endothelial cells (BEC) in vitro. We analyzed the possible stabilizing effect of MK801, a highly selective N-methyl-d-aspartate receptor (NMDAR) antagonist, on BBB integrity. Levels of reactive oxygen species (ROS), glutamate (Glut) release and monocyte adhesion were measured under normoxia and H/R. BBB integrity was monitored measuring the trans-endothelial electrical resistance (TEER). TEER values dropped under H/R conditions which was abolished by MK801. Glut release from astrocytes, but not from endothelial cells was significantly increased under H/R, as were ROS levels and monocyte adhesion. The oxidative stress was blocked by MK801 and the NAD(P)H-oxidase inhibitor apocynin. We observed that calcium (Ca(2+)) signaling plays a crucial role during ROS generation and monocyte adhesion under H/R. ROS levels were decreased by applying ryanodine, a blocker of Ca(2+) release from the endoplasmic reticulum (ER) and by lowering the extracellular Ca(2+) concentration. Xestospongin C, which blocks IP(3) mediated Ca(2+) release from the ER did not alter ROS production under H/R conditions. These findings indicate that both extracellular Ca(2+) influx and ryanodine-mediated intracellular Ca(2+) release from the ER during H/R contribute to ROS formation at the BBB. Blocking ROS or Ca(2+) signaling prevented H/R-induced monocyte adhesion to BEC. We conclude, that the activation of NMDAR under H/R by Glut increases intracellular Ca(2+) levels, contributes to BBB disruption, ROS generation and monocyte adhesion. | lld:pubmed |
| pubmed-article:18996441 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18996441 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18996441 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18996441 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18996441 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18996441 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18996441 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18996441 | pubmed:issn | 0304-3940 | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:FriedlPeterP | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:LuhmannHeiko... | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:KuhlmannChris... | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:GerigkMarlisM | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:BenderBiancaB | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:CloshenDoroth... | lld:pubmed |
| pubmed-article:18996441 | pubmed:author | pubmed-author:ZehendnerChri... | lld:pubmed |
| pubmed-article:18996441 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18996441 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:18996441 | pubmed:volume | 449 | lld:pubmed |
| pubmed-article:18996441 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18996441 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18996441 | pubmed:pagination | 168-72 | lld:pubmed |
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| pubmed-article:18996441 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:18996441 | pubmed:articleTitle | MK801 blocks hypoxic blood-brain-barrier disruption and leukocyte adhesion. | lld:pubmed |
| pubmed-article:18996441 | pubmed:affiliation | Institute of Physiology and Pathophysiology, Johannes Gutenberg University of Mainz, Duesbergweg 6, 55128 Mainz, Germany. SuC.Kuhlmann@t-online.de | lld:pubmed |
| pubmed-article:18996441 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18996441 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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