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J. Biol. Chem., Vol. 277, Issue 43, 40575-40582, October 25, 2002
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From the Leukocyte migration to sites of inflammation is a
multistep process involving transient adhesion to the endothelium
followed by cell surface-controlled proteolysis for transmigration
through the vessel wall and chemotactic movement within tissues. One of the key players in this machinery appears to be the urokinase-type plasminogen activator (uPA)/uPA receptor system. The role of uPA and
its receptor (CD87) in plasminogen (Plg) activation, cell adhesion, and
chemotaxis is well established; however, less is known of how these
activities are regulated. Here we provide evidence that the mannose
6-phosphate/insulin-like growth factor 2 receptor (CD222) controls
CD87-mediated functions. Expression of human CD222 in CD222
The N Terminus of Mannose 6-Phosphate/Insulin-like Growth Factor
2 Receptor in Regulation of Fibrinolysis and Cell Migration*
,,
,**
Institute of Immunology, Vienna
International Research Cooperation Center at Novartis
Forschungs-institut, University of Vienna, Vienna A-1235, Austria, the
§ Institute of Molecular Genetics, Academy of Sciences of
the Czech Republic, Prague 4-14220, Czech Republic, the
¶ Department of Vascular Biology and Thrombosis Research,
University of Vienna, Vienna A-1090, Austria, and Roche
Diagnostics, Division Pharma, Penzberg D-82372, Germany
/ mouse
fibroblasts down-regulated Plg activation, cell adhesion, and
chemotaxis induced by the uPA/CD87 system. In addition, we demonstrate
that the N-terminal region of CD222, which is similar to the
Plg-binding site of streptokinase, plays a crucial role in binding of
CD87 and Plg. A peptide derived from this region in CD222 is able to
disrupt the physical interaction of CD222 with CD87 and, furthermore,
mimics the inhibitory effects of CD222 on CD87 functions. Taken
together, our results indicate a novel role for CD222 in
regulation of fibrinolysis, cell adhesion, and migration.
*
This work was supported by the Austrian Science Fund. Part
of the work was performed within the Biomolecular Therapeutics Research Consortium.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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