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10.1038/ncomms10493 http://scihub22266oqcxt.onion/10.1038/ncomms10493 C4737874!4737874 !26814335     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26814335 &cmd=llinks): Failed to open stream: HTTP request failed! 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F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling |pdf=|usr=}}{{26814335 }} gab.com Text F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26814335 #FOAvip During immune surveillance and inflammation, leukocytes exit the vasculature through transient openings in the endothelium without causing plasma leakage. However, the exact mechanisms behind this intriguing phenomenon are still unknown. Here we report that maintenance of endothelial barrier integrity during leukocyte diapedesis requires local endothelial RhoA cycling. Endothelial RhoA depletion in vitro or Rho inhibition in vivo provokes neutrophil-induced vascular leakage that manifests during the physical movement of neutrophils through the endothelial layer. Local RhoA activation initiates the formation of contractile F-actin structures that surround emigrating neutrophils. These structures that surround neutrophil-induced endothelial pores prevent plasma leakage through actomyosin-based pore confinement. Mechanistically, we found that the initiation of RhoA activity involves ICAM-1 and the Rho GEFs Ect2 and LARG. In addition, regulation of actomyosin-based endothelial pore confinement involves ROCK2b, but not ROCK1. Thus, endothelial cells assemble RhoA-controlled contractile F-actin structures around endothelial pores that prevent vascular leakage during leukocyte extravasation. Twit Text FOAVip F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26814335 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26814335 #FOAvip English Wikipedia <ref>{{Cite pmid|26814335 }}</ref> F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling #MMPMID26814335 Heemskerk N ; Schimmel L ; Oort C ; van Rijssel J ; Yin T ; Ma B ; van Unen J ; Pitter B ; Huveneers S ; Goedhart J ; Wu Y ; Montanez E ; Woodfin A ; van Buul JD Nat Commun 2016[Jan]; 7 (ä): 10493 PMID26814335 show ga During immune surveillance and inflammation, leukocytes exit the vasculature through transient openings in the endothelium without causing plasma leakage. However, the exact mechanisms behind this intriguing phenomenon are still unknown. Here we report that maintenance of endothelial barrier integrity during leukocyte diapedesis requires local endothelial RhoA cycling. Endothelial RhoA depletion in vitro or Rho inhibition in vivo provokes neutrophil-induced vascular leakage that manifests during the physical movement of neutrophils through the endothelial layer. Local RhoA activation initiates the formation of contractile F-actin structures that surround emigrating neutrophils. These structures that surround neutrophil-induced endothelial pores prevent plasma leakage through actomyosin-based pore confinement. Mechanistically, we found that the initiation of RhoA activity involves ICAM-1 and the Rho GEFs Ect2 and LARG. In addition, regulation of actomyosin-based endothelial pore confinement involves ROCK2b, but not ROCK1. Thus, endothelial cells assemble RhoA-controlled contractile F-actin structures around endothelial pores that prevent vascular leakage during leukocyte extravasation. |*Signal Transduction [MESH] |*Transendothelial and Transepithelial Migration [MESH] |Actin Cytoskeleton/chemistry/metabolism [MESH] |Actins/genetics/*metabolism [MESH] |Animals [MESH] |Capillary Permeability [MESH] |Cells, Cultured [MESH] |Endothelium, Vascular/cytology/*metabolism [MESH] |Human Umbilical Vein Endothelial Cells/*cytology/metabolism [MESH] |Humans [MESH] |Intercellular Adhesion Molecule-1 [MESH] |Leukocytes/*cytology/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neutrophils/cytology/metabolism [MESH]F-actin-rich contractile endothelial pores prevent vascular leakage du(epmc).pdf DeepDyve Pubget Overpricing