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10.1073/pnas.1717489115 http://scihub22266oqcxt.onion/10.1073/pnas.1717489115 C5776826!5776826 !29255056     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29255056 &cmd=llinks): Failed to open stream: HTTP request failed! 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Three-dimensional forces exerted by leukocytes and vascular endothelial cells dynamically facilitate diapedesis |pdf=|usr=}}{{29255056 }} gab.com Text Three-dimensional forces exerted by leukocytes and vascular endothelial cells dynamically facilitate diapedesis JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29255056 #FOAvip Leukocyte transmigration across vessel walls is a critical step in the innate immune response. Upon their activation and firm adhesion to vascular endothelial cells (VECs), leukocytes preferentially extravasate across junctional gaps in the endothelial monolayer (paracellular diapedesis). It has been hypothesized that VECs facilitate paracellular diapedesis by opening their cell-cell junctions in response to the presence of an adhering leukocyte. However, it is unclear how leukocytes interact mechanically with VECs to open the VEC junctions and migrate across the endothelium. In this study, we measured the spatial and temporal evolution of the 3D traction stresses generated by the leukocytes and VECs to elucidate the sequence of mechanical events involved in paracellular diapedesis. Our measurements suggest that the contractile stresses exerted by the leukocytes and the VECs can separately perturb the junctional tensions of VECs to result in the opening of gaps before the initiation of leukocyte transmigration. Decoupling the stresses exerted by the transmigrating leukocytes and the VECs reveals that the leukocytes actively contract the VECs to open a junctional gap and then push themselves across the gap by generating strong stresses that push into the matrix. In addition, we found that diapedesis is facilitated when the tension fluctuations in the VEC monolayer were increased by proinflammatory thrombin treatment. Our findings demonstrate that diapedesis can be mechanically regulated by the transmigrating leukocytes and by proinflammatory signals that increase VEC contractility. Twit Text FOAVip Three-dimensional forces exerted by leukocytes and vascular endothelial cells dynamically facilitate diapedesis ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=29255056 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29255056 #FOAvip English Wikipedia <ref>{{Cite pmid|29255056 }}</ref> Three-dimensional forces exerted by leukocytes and vascular endothelial cells dynamically facilitate diapedesis #MMPMID29255056 Yeh YT ; Serrano R ; François J ; Chiu JJ ; Li YJ ; Del Álamo JC ; Chien S ; Lasheras JC Proc Natl Acad Sci U S A 2018[Jan]; 115 (1 ): 133-138 PMID29255056 show ga Leukocyte transmigration across vessel walls is a critical step in the innate immune response. Upon their activation and firm adhesion to vascular endothelial cells (VECs), leukocytes preferentially extravasate across junctional gaps in the endothelial monolayer (paracellular diapedesis). It has been hypothesized that VECs facilitate paracellular diapedesis by opening their cell-cell junctions in response to the presence of an adhering leukocyte. However, it is unclear how leukocytes interact mechanically with VECs to open the VEC junctions and migrate across the endothelium. In this study, we measured the spatial and temporal evolution of the 3D traction stresses generated by the leukocytes and VECs to elucidate the sequence of mechanical events involved in paracellular diapedesis. Our measurements suggest that the contractile stresses exerted by the leukocytes and the VECs can separately perturb the junctional tensions of VECs to result in the opening of gaps before the initiation of leukocyte transmigration. Decoupling the stresses exerted by the transmigrating leukocytes and the VECs reveals that the leukocytes actively contract the VECs to open a junctional gap and then push themselves across the gap by generating strong stresses that push into the matrix. In addition, we found that diapedesis is facilitated when the tension fluctuations in the VEC monolayer were increased by proinflammatory thrombin treatment. Our findings demonstrate that diapedesis can be mechanically regulated by the transmigrating leukocytes and by proinflammatory signals that increase VEC contractility. |*Models, Biological [MESH] |HL-60 Cells [MESH] |Human Umbilical Vein Endothelial Cells/cytology/*metabolism [MESH] |Humans [MESH] |Intercellular Junctions/*metabolism [MESH] |Leukocytes/cytology/*metabolism [MESH]Three-dimensional forces exerted by leukocytes and vascular endothelia(epmc).pdf DeepDyve Pubget Overpricing