H Zhang1, R W Colman, N Sheng. 1. The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA.
Abstract
OBJECTIVE AND DESIGN: The goal of this study is to investigate the consequence of the interaction between Mac-1 and uPAR and determine the mechanisms by which uPAR regulates Mac-1 dependent adhesion to fibrinogen. MATERIAL: Human embryonic kidney 293 cells transfected with Mac-1 or uPAR or co-transfected with both Mac-1 and uPAR. METHODS: Cell adhesion and binding assays and Western Blotting for protein tyrosine phosphorylation analysis. RESULTS: The adhesion to fibrinogen was increased two-fold for Mac-1-uPAR co-transfected cells comparing to the Mac-1 transfected cells alone. The increased adhesion was inhibited when cells were treated with phosphatidylinositol-specific phospholipase C to remove uPAR. Occupancy of uPAR with urokinase-type plasminogen activator further enhanced the cell adhesion to fibrinogen. Phosphorylation of focal adhesion kinase (FAK) and mitogen-activated protein kinase (MAPK) was increased in Mac-1-uPAR co-transfected cells but not in Mac-1 transfected cells. CONCLUSIONS: uPAR up-regulated the Mac-1 adhesion to fibrinogen and FAK and MAPK were involved in this regulation.
OBJECTIVE AND DESIGN: The goal of this study is to investigate the consequence of the interaction between Mac-1 and uPAR and determine the mechanisms by which uPAR regulates Mac-1 dependent adhesion to fibrinogen. MATERIAL: Humanembryonic kidney 293 cells transfected with Mac-1 or uPAR or co-transfected with both Mac-1 and uPAR. METHODS: Cell adhesion and binding assays and Western Blotting for protein tyrosine phosphorylation analysis. RESULTS: The adhesion to fibrinogen was increased two-fold for Mac-1-uPAR co-transfected cells comparing to the Mac-1 transfected cells alone. The increased adhesion was inhibited when cells were treated with phosphatidylinositol-specific phospholipase C to remove uPAR. Occupancy of uPAR with urokinase-type plasminogen activator further enhanced the cell adhesion to fibrinogen. Phosphorylation of focal adhesion kinase (FAK) and mitogen-activated protein kinase (MAPK) was increased in Mac-1-uPAR co-transfected cells but not in Mac-1 transfected cells. CONCLUSIONS:uPAR up-regulated the Mac-1 adhesion to fibrinogen and FAK and MAPK were involved in this regulation.
Authors: Mohammad M Khan; Harlan N Bradford; Irma Isordia-Salas; Yuchuan Liu; Yi Wu; Ricardo G Espinola; Berhane Ghebrehiwet; Robert W Colman Journal: Arterioscler Thromb Vasc Biol Date: 2006-08-10 Impact factor: 8.311
Authors: Kerstin Göbel; Susann Pankratz; Chloi-Magdalini Asaridou; Alexander M Herrmann; Stefan Bittner; Monika Merker; Tobias Ruck; Sarah Glumm; Friederike Langhauser; Peter Kraft; Thorsten F Krug; Johanna Breuer; Martin Herold; Catharina C Gross; Denise Beckmann; Adelheid Korb-Pap; Michael K Schuhmann; Stefanie Kuerten; Ioannis Mitroulis; Clemens Ruppert; Marc W Nolte; Con Panousis; Luisa Klotz; Beate Kehrel; Thomas Korn; Harald F Langer; Thomas Pap; Bernhard Nieswandt; Heinz Wiendl; Triantafyllos Chavakis; Christoph Kleinschnitz; Sven G Meuth Journal: Nat Commun Date: 2016-05-18 Impact factor: 14.919