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J. Biol. Chem., Vol. 277, Issue 42, 39833-39839, October 18, 2002
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From the SHPS-1 is a receptor-type glycoprotein that binds
and activates the protein-tyrosine phosphatases SHP-1 and SHP-2, and
thereby negatively modulates intracellular signaling initiated by
various cell surface receptors coupled to tyrosine kinases. SHPS-1 also regulates intercellular communication in the neural and immune systems
through its association with CD47 (integrin-associated protein) on
adjacent cells. Furthermore, recent studies with fibroblasts derived
from mice expressing an SHPS-1 mutant that lacks most of the
cytoplasmic region suggested that the intact protein contributes to
cytoskeletal function. Mice homozygous for this SHPS-1 mutation have
now been shown to manifest thrombocytopenia. These animals did not
exhibit a defect in megakaryocytopoiesis or in platelet production.
However, platelets were cleared from the bloodstream more rapidly in
the mutant mice than in wild-type animals. Furthermore, peritoneal
macrophages from the mutant mice phagocytosed red blood cells more
effectively than did those from wild-type mice; in addition, they
exhibited an increase both in the rate of cell spreading and in the
formation of filopodia-like structures at the cell periphery. These
results indicate that SHPS-1 both contributes to the survival of
circulating platelets and down-regulates the macrophage phagocytic response.
Negative Regulation of Platelet Clearance and of the Macrophage
Phagocytic Response by the Transmembrane Glycoprotein SHPS-1*
,§,
,,,,,,
Division of Diabetes, Digestive, and Kidney
Diseases, Department of Clinical Molecular Medicine, and
§§ Division of Surgical Pathology, Department of
Biomedical Informatics, Kobe University Graduate School of Medicine,
7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan, the
¶ Department of Host Defense, Research Institute for Microbial
Diseases, Osaka University, Suita 565-0871, Japan,
Pharmaceutical Development Laboratories and
** Pharmaceutical Research Laboratories, Kirin Brewery Co.,
Ltd., Takasaki 370-1295, Japan, and the
Biosignal Research Center, Institute for
Molecular and Cellular Regulation, Gunma University,
Maebashi 371-8512, Japan
*
This work was supported by a grant-in-aid for cancer
research and a grant-in-aid for scientific research from the Ministry of Education, Science, Sports, and Culture of Japan, and by a grant-in-aid from the Research for the Future Program of the Japan Society for the Promotion of Science.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.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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