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10.4049/jimmunol.1400700 http://scihub22266oqcxt.onion/10.4049/jimmunol.1400700 C4138548!4138548 !25063869     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25063869 &cmd=llinks): Failed to open stream: HTTP request failed! 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Rapid remodeling of tight junctions during paracellular diapedesis in a human model of the blood-brain barrier |pdf=|usr=}}{{25063869 }} gab.com Text Rapid remodeling of tight junctions during paracellular diapedesis in a human model of the blood-brain barrier JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25063869 #FOAvip Leukocyte transendothelial migration (TEM; diapedesis) is a critical event in immune surveillance and inflammation. Most TEM occurs at endothelial cell borders (paracellular). However, there is indirect evidence to suggest that, at the tight junctions of the blood-brain barrier (BBB), leukocytes migrate directly through the endothelial cell body (transcellular). Why leukocytes migrate through the endothelial cell body rather than the cell borders is unknown. To test the hypothesis that the tightness of endothelial cell junctions influences the pathway of diapedesis, we developed an in vitro model of the BBB that possessed 10-fold higher electrical resistance than standard culture conditions and strongly expressed the BBB tight junction proteins claudin-5 and claudin-3. We found that paracellular TEM was still the predominant pathway (?98%) and TEM was dependent on PECAM-1 and CD99. We show that endothelial tight junctions expressing claudin-5 are dynamic and undergo rapid remodeling during TEM. Membrane from the endothelial lateral border recycling compartment is mobilized to the exact site of tight junction remodeling. This preserves the endothelial barrier by sealing the intercellular gaps with membrane and engaging the migrating leukocyte with unligated adhesion molecules (PECAM-1 and CD99) as it crosses the cell border. These findings provide new insights into leukocyte-endothelial interactions at the BBB and suggest that tight junctions are more dynamic than previously appreciated. Twit Text FOAVip Rapid remodeling of tight junctions during paracellular diapedesis in a human model of the blood-brain barrier ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25063869 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25063869 #FOAvip English Wikipedia <ref>{{Cite pmid|25063869 }}</ref> Rapid remodeling of tight junctions during paracellular diapedesis in a human model of the blood-brain barrier #MMPMID25063869 Winger RC ; Koblinski JE ; Kanda T ; Ransohoff RM ; Muller WA J Immunol 2014[Sep]; 193 (5 ): 2427-37 PMID25063869 show ga Leukocyte transendothelial migration (TEM; diapedesis) is a critical event in immune surveillance and inflammation. Most TEM occurs at endothelial cell borders (paracellular). However, there is indirect evidence to suggest that, at the tight junctions of the blood-brain barrier (BBB), leukocytes migrate directly through the endothelial cell body (transcellular). Why leukocytes migrate through the endothelial cell body rather than the cell borders is unknown. To test the hypothesis that the tightness of endothelial cell junctions influences the pathway of diapedesis, we developed an in vitro model of the BBB that possessed 10-fold higher electrical resistance than standard culture conditions and strongly expressed the BBB tight junction proteins claudin-5 and claudin-3. We found that paracellular TEM was still the predominant pathway (?98%) and TEM was dependent on PECAM-1 and CD99. We show that endothelial tight junctions expressing claudin-5 are dynamic and undergo rapid remodeling during TEM. Membrane from the endothelial lateral border recycling compartment is mobilized to the exact site of tight junction remodeling. This preserves the endothelial barrier by sealing the intercellular gaps with membrane and engaging the migrating leukocyte with unligated adhesion molecules (PECAM-1 and CD99) as it crosses the cell border. These findings provide new insights into leukocyte-endothelial interactions at the BBB and suggest that tight junctions are more dynamic than previously appreciated. |*Models, Cardiovascular [MESH] |12E7 Antigen [MESH] |Antigens, CD/immunology [MESH] |Blood-Brain Barrier/cytology/*immunology [MESH] |Cell Adhesion Molecules/immunology [MESH] |Claudin-3/immunology [MESH] |Claudin-5/immunology [MESH] |Human Umbilical Vein Endothelial Cells/cytology/*immunology [MESH] |Humans [MESH] |Platelet Endothelial Cell Adhesion Molecule-1/immunology [MESH] |Tight Junctions/*immunology [MESH]Rapid remodeling of tight junctions during paracellular diapedesis in (epmc).pdf DeepDyve Pubget Overpricing