Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Home
Search
Quick Search
Advanced
Fulltext
Browse
Collections
Persons
My eDoc
Session History
Login
Name:
Password:
Documentation
Help
Support Wiki
Direct access to
document ID:


          Institute: MPI für molekulare Biomedizin     Collection: Jahrbuch 2018 (publ. 2017, arch)     Display Documents



  history
ID: 744101.0, MPI für molekulare Biomedizin / Jahrbuch 2018 (publ. 2017, arch)
Endothelial Basement Membrane Laminin 511 Contributes to Endothelial Junctional Tightness and Thereby Inhibits Leukocyte Transmigration
Authors:Song, J.; Zhang, X.; Buscher, K.; Wang, Y.; Wang, H.; Di Russo, J.; Li, L.; Lutke-Enking, S.; Zarbock, A.; Stadtmann, A.; Striewski, P.; Wirth, B.; Kuzmanov, I.; Wiendl, H.; Schulte, D.; Vestweber, D.; Sorokin, L.
Date of Publication (YYYY-MM-DD):2017-01-31
Title of Journal:Cell Rep
Volume:18
Issue / Number:5
Start Page:1256
End Page:1269
Review Status:Internal review
Audience:Not Specified
Abstract / Description:Endothelial basement membranes constitute barriers to extravasating leukocytes during inflammation, a process where laminin isoforms define sites of leukocyte exit; however, how this occurs is poorly understood. In addition to a direct effect on leukocyte transmigration, we show that laminin 511 affects endothelial barrier function by stabilizing VE-cadherin at junctions and downregulating expression of CD99L2, correlating with reduced neutrophil extravasation. Binding of endothelial cells to laminin 511, but not laminin 411 or non-endothelial laminin 111, enhanced transendothelial cell electrical resistance (TEER) and inhibited neutrophil transmigration. Data suggest that endothelial adhesion to laminin 511 via beta1 and beta3 integrins mediates RhoA-induced VE-cadherin localization to cell-cell borders, and while CD99L2 downregulation requires integrin beta1, it is RhoA-independent. Our data demonstrate that molecular information provided by basement membrane laminin 511 affects leukocyte extravasation both directly and indirectly by modulating endothelial barrier properties.
Free Keywords:Animals; Antigens, CD/metabolism; Basement Membrane/*metabolism; Cadherins/metabolism; Cell Adhesion/physiology; Cell Movement/*physiology; Cells, Cultured; Endothelial Cells/*metabolism; Endothelium, Vascular/*metabolism; Laminin/*metabolism; Leukocytes/*metabolism; Male; Mice; Mice, Knockout; Neutrophils/metabolism/physiology; *VE-cadherin; *endothelial basement membrane; *laminin; *neutrophil extravasation
External Publication Status:published
Document Type:Article
Communicated by:MPI für molekulare Biomedizin
Affiliations:MPI für molekulare Biomedizin
External Affiliations:Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany; Department of Anesthesiology and Intensive Care Medicine, University of Muenster, 48149 Muenster, Germany. Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany; Institute for Computational and Applied Mathematics, University of Muenster, 48149 Muenster, Germany. Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany; Department of Neurology, University Hospital of Muenster, University of Muenster, 48149 Muenster, Germany. Max-Planck Institute of Molecular Biomedicine, 48149 Muenster, Germany. Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany; Max-Planck Institute of Molecular Biomedicine, 48149 Muenster, Germany. Institute of Physiological Chemistry and Pathobiochemistry, University of Muenster, 48149 Muenster, Germany; Cells-in-Motion Cluster of Excellence, University of Muenster, 48149 Muenster, Germany. Electronic address: sorokin@uni-muenster.de.
Identifiers:ISSN:2211-1247 (Electronic) %R 10.1016/j.celrep.2016.12... [ID No:1]
URL:https://www.ncbi.nlm.nih.gov/pubmed/28147279 [ID No:2]
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.