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J. Biol. Chem., Vol. 275, Issue 31, 23998-24002, August 4, 2000
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From the Department of Molecular Oncology, General Surgery,
University of Witten-Herdecke, 42283 Wuppertal and the
§ Department of Clinical Immunology, Hannover Medical
School, 30625 Hannover, Germany
Platelet glycoprotein (GP) VI has been proposed
as the major collagen receptor for activation of human platelets. Human
GPVI belongs to the immunoglobulin superfamily and is noncovalently associated with the FcR
Expression and Function of the Mouse Collagen Receptor
Glycoprotein VI Is Strictly Dependent on Its Association with the
FcR
Chain*
,
chain that is involved in signaling through the receptor. In mice, similar mechanisms seem to exist as platelets from FcR chain-deficient mice do not aggregate in response to collagen. However, the activating collagen receptor on mouse platelets has not been definitively identified. In the current study we examined
the function and in vivo expression of GPVI in control and
FcR chain-deficient mice with the first monoclonal antibody against
GPVI (JAQ1). On wild type platelets, JAQ1 inhibited platelet aggregation induced by collagen but not PMA or thrombin. Cross-linking of bound JAQ1, on the other hand, induced aggregation of wild type but
not FcR chain-deficient platelets. JAQ1 stained platelets and
megakaryocytes from wild type but not FcR chain-deficient mice.
Furthermore, JAQ1 recognized GPVI (approximately 60 kDa) in
immunoprecipitation and Western blot experiments with wild type but not
FcR chain-deficient platelets. These results strongly suggest that
GPVI is the collagen receptor responsible for platelet activation in
mice and demonstrate that the association with the FcR chain is
critical for its expression and function.
*
This work was supported in part by Grant Ni 556/2-1 (to
B. N. and J. E. G.) from the Deutsche Forschungsgemeinschaft and the BAYER AG.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.
To whom correspondence should be addressed: IMMI, Klinikum
Wuppertal, Universität Witten-Herdecke, Heusnerstrasse 40, D-42283 Wuppertal, Germany. Tel.: 49-2332-666 860; Fax: 9-2332-666 861; E-mail: nieswand@klinikum-wuppertal.de.
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R. K. Andrews, E. E. Gardiner, N. Asazuma, O. Berlanga, D. Tulasne, B. Nieswandt, A. I. Smith, M. C. Berndt, and S. P. Watson A Novel Viper Venom Metalloproteinase, Alborhagin, Is an Agonist at the Platelet Collagen Receptor GPVI J. Biol. Chem., July 20, 2001; 276(30): 28092 - 28097. [Abstract] [Full Text] [PDF]
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