Regulation of CD11b/CD18 (Mac-1) adhesion to fibrinogen by urokinase receptor (uPAR)

被引：0

作者：

H. Zhang

R. W. Colman

N. Sheng

机构：

[1] The Sol Sherry Thrombosis Research Center,

[2] Temple University School of Medicine,undefined

[3] 3400 North Broad Street,undefined

[4] Philadelphia,undefined

[5] PA 19140,undefined

[6] USA,undefined

[7] Fax: ++215 707 2783,undefined

[8] e-mail: ,undefined

[9] University of Houston,undefined

[10] Department of Chemistry,undefined

[11] 136 Fleming,undefined

[12] Houston,undefined

[13] TX 77204-5003,undefined

[14] USA,undefined

[15] Fax: ++713 743 2709,undefined

[16] e-mail: ,undefined

来源：

Inflammation Research | 2003年 / 52卷

关键词：

Key words: Focal adhesion kinase – Mitogen-activated protein kinase – Urokinase;

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学科分类号：

摘要：

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.

引用

页码：86 / 93

页数：7