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10.1371/journal.pone.0120075 http://scihub22266oqcxt.onion/10.1371/journal.pone.0120075 C4376850!4376850 !25816133     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25816133 &cmd=llinks): Failed to open stream: HTTP request failed! 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Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF-?B-dependent phases |pdf=|usr=}}{{25816133 }} gab.com Text Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF- B-dependent phases JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25816133 #FOAvip Capillary leak in severe sepsis involves disruption of endothelial cell tight junctions. We modeled this process by TNF treatment of cultured human dermal microvascular endothelial cell (HDMEC) monolayers, which unlike human umbilical vein endothelial cells form claudin-5-dependent tight junctions and a high-resistance permeability barrier. Continuous monitoring with electrical cell-substrate impedance sensing revealed that TNF disrupts tight junction-dependent HDMEC barriers in discrete steps: an ~5% increase in transendothelial electrical resistance over 40 minutes; a decrease to ~10% below basal levels over 2 hours (phase 1 leak); an interphase plateau of 1 hour; and a major fall in transendothelial electrical resistance to < 70% of basal levels by 8-10 hours (phase 2 leak), with EC50 values of TNF for phase 1 and 2 leak of ~30 and ~150 pg/ml, respectively. TNF leak is reversible and independent of cell death. Leak correlates with disruption of continuous claudin-5 immunofluorescence staining, myosin light chain phosphorylation and loss of claudin-5 co-localization with cortical actin. All these responses require NF-?B signaling, shown by inhibition with Bay 11 or overexpression of I?B super-repressor, and are blocked by H-1152 or Y-27632, selective inhibitors of Rho-associated kinase that do not block other NF-?B-dependent responses. siRNA combined knockdown of Rho-associated kinase-1 and -2 also prevents myosin light chain phosphorylation, loss of claudin-5/actin co-localization, claudin-5 reorganization and reduces phase 1 leak. However, unlike H-1152 and Y-27632, combined Rho-associated kinase-1/2 siRNA knockdown does not reduce the magnitude of phase 2 leak, suggesting that H-1152 and Y-27632 have targets beyond Rho-associated kinases that regulate endothelial barrier function. We conclude that TNF disrupts TJs in HDMECs in two distinct NF-?B-dependent steps, the first involving Rho-associated kinase and the second likely to involve an as yet unidentified but structurally related protein kinase(s). Twit Text FOAVip Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF- B-dependent phases ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25816133 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25816133 #FOAvip English Wikipedia <ref>{{Cite pmid|25816133 }}</ref> Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF-?B-dependent phases #MMPMID25816133 Clark PR ; Kim RK ; Pober JS ; Kluger MS PLoS One 2015[]; 10 (3 ): e0120075 PMID25816133 show ga Capillary leak in severe sepsis involves disruption of endothelial cell tight junctions. We modeled this process by TNF treatment of cultured human dermal microvascular endothelial cell (HDMEC) monolayers, which unlike human umbilical vein endothelial cells form claudin-5-dependent tight junctions and a high-resistance permeability barrier. Continuous monitoring with electrical cell-substrate impedance sensing revealed that TNF disrupts tight junction-dependent HDMEC barriers in discrete steps: an ~5% increase in transendothelial electrical resistance over 40 minutes; a decrease to ~10% below basal levels over 2 hours (phase 1 leak); an interphase plateau of 1 hour; and a major fall in transendothelial electrical resistance to < 70% of basal levels by 8-10 hours (phase 2 leak), with EC50 values of TNF for phase 1 and 2 leak of ~30 and ~150 pg/ml, respectively. TNF leak is reversible and independent of cell death. Leak correlates with disruption of continuous claudin-5 immunofluorescence staining, myosin light chain phosphorylation and loss of claudin-5 co-localization with cortical actin. All these responses require NF-?B signaling, shown by inhibition with Bay 11 or overexpression of I?B super-repressor, and are blocked by H-1152 or Y-27632, selective inhibitors of Rho-associated kinase that do not block other NF-?B-dependent responses. siRNA combined knockdown of Rho-associated kinase-1 and -2 also prevents myosin light chain phosphorylation, loss of claudin-5/actin co-localization, claudin-5 reorganization and reduces phase 1 leak. However, unlike H-1152 and Y-27632, combined Rho-associated kinase-1/2 siRNA knockdown does not reduce the magnitude of phase 2 leak, suggesting that H-1152 and Y-27632 have targets beyond Rho-associated kinases that regulate endothelial barrier function. We conclude that TNF disrupts TJs in HDMECs in two distinct NF-?B-dependent steps, the first involving Rho-associated kinase and the second likely to involve an as yet unidentified but structurally related protein kinase(s). |Cell Membrane Permeability [MESH] |Cells, Cultured [MESH] |Claudin-5/*metabolism [MESH] |Dermis/cytology/*metabolism [MESH] |Endothelium, Vascular/cytology/*metabolism [MESH] |Human Umbilical Vein Endothelial Cells/cytology/*metabolism [MESH] |Humans [MESH] |Microscopy, Fluorescence [MESH] |Myosin Light Chains/metabolism [MESH] |Myosin-Light-Chain Kinase/metabolism [MESH] |NF-kappa B/*metabolism [MESH] |Phosphorylation [MESH] |RNA, Small Interfering/genetics [MESH] |Signal Transduction/drug effects [MESH] |Tight Junctions/*metabolism [MESH] |Tumor Necrosis Factor-alpha/*pharmacology [MESH]Tumor necrosis factor disrupts claudin-5 endothelial tight junction ba(epmc).pdf DeepDyve Pubget Overpricing