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10.1002/jcp.26064 http://scihub22266oqcxt.onion/10.1002/jcp.26064 C5655747!5655747 !28639275     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28639275 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       J+Cell+Physiol 2018 ; 233 (1 ): 186-200 Nephropedia Template TP {{tp|p=28639275 |t=2018. Statin regulated ERK5 stimulates tight junction formation and reduces permeability in human cardiac endothelial cells |pdf=|usr=}}{{28639275 }} gab.com Text Statin regulated ERK5 stimulates tight junction formation and reduces permeability in human cardiac endothelial cells JO: J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28639275 #FOAvip The MEKK3/MEK5/ERK5 signaling axis is required for cardiovascular development in vivo. We analyzed the physiological role of ERK5 in cardiac endothelial cells and the consequence of activation of this kinase by the statin class of HMG Co-A reductase inhibitor drugs. We utilized human cardiac microvascular endothelial cells (HCMECs) and altered ERK5 expression using siRNA mediated gene silencing or overexpression of constitutively active MEK5 and ERK5 to reveal a role for ERK5 in regulating endothelial tight junction formation and cell permeability. Statin treatment of HCMECs stimulated activation of ERK5 and translocation to the plasma membrane resulting in co-localization with the tight junction protein ZO-1 and a concomitant reduction in endothelial cell permeability. Statin mediated activation of ERK5 was a consequence of reduced isoprenoid synthesis following HMG Co-A reductase inhibition. Statin pretreatment could overcome the effect of doxorubicin in reducing endothelial tight junction formation and prevent increased permeability. Our data provide the first evidence for the role of ERK5 in regulating endothelial tight junction formation and endothelial cell permeability. Statin mediated ERK5 activation and the resulting decrease in cardiac endothelial cell permeability may contribute to the cardioprotective effects of statins in reducing doxorubicin-induced cardiotoxicity. Twit Text FOAVip Statin regulated ERK5 stimulates tight junction formation and reduces permeability in human cardiac endothelial cells ????J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28639275 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28639275 #FOAvip English Wikipedia <ref>{{Cite pmid|28639275 }}</ref> Statin regulated ERK5 stimulates tight junction formation and reduces permeability in human cardiac endothelial cells #MMPMID28639275 Wilkinson EL ; Sidaway JE ; Cross MJ J Cell Physiol 2018[Jan]; 233 (1 ): 186-200 PMID28639275 show ga The MEKK3/MEK5/ERK5 signaling axis is required for cardiovascular development in vivo. We analyzed the physiological role of ERK5 in cardiac endothelial cells and the consequence of activation of this kinase by the statin class of HMG Co-A reductase inhibitor drugs. We utilized human cardiac microvascular endothelial cells (HCMECs) and altered ERK5 expression using siRNA mediated gene silencing or overexpression of constitutively active MEK5 and ERK5 to reveal a role for ERK5 in regulating endothelial tight junction formation and cell permeability. Statin treatment of HCMECs stimulated activation of ERK5 and translocation to the plasma membrane resulting in co-localization with the tight junction protein ZO-1 and a concomitant reduction in endothelial cell permeability. Statin mediated activation of ERK5 was a consequence of reduced isoprenoid synthesis following HMG Co-A reductase inhibition. Statin pretreatment could overcome the effect of doxorubicin in reducing endothelial tight junction formation and prevent increased permeability. Our data provide the first evidence for the role of ERK5 in regulating endothelial tight junction formation and endothelial cell permeability. Statin mediated ERK5 activation and the resulting decrease in cardiac endothelial cell permeability may contribute to the cardioprotective effects of statins in reducing doxorubicin-induced cardiotoxicity. |Antibiotics, Antineoplastic/toxicity [MESH] |Capillary Permeability/*drug effects [MESH] |Cardiotoxicity [MESH] |Cells, Cultured [MESH] |Coronary Vessels/*drug effects/enzymology [MESH] |Cytoprotection [MESH] |Dose-Response Relationship, Drug [MESH] |Doxorubicin/toxicity [MESH] |Endothelial Cells/*drug effects/enzymology [MESH] |Enzyme Activation [MESH] |Heart Diseases/chemically induced/enzymology/genetics/*prevention & control [MESH] |Humans [MESH] |Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology [MESH] |Mitogen-Activated Protein Kinase 7/genetics/*metabolism [MESH] |Protein Prenylation/drug effects [MESH] |Protein Transport/drug effects [MESH] |Quinolines/pharmacology [MESH] |RNA Interference [MESH] |Rosuvastatin Calcium/pharmacology [MESH] |Signal Transduction/drug effects [MESH] |Simvastatin/pharmacology [MESH] |Tight Junctions/*drug effects/enzymology [MESH] |Transfection [MESH]Statin regulated ERK5 stimulates tight junction formation and reduces (epmc).pdf DeepDyve Pubget Overpricing