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Originally published In Press as doi:10.1074/jbc.M104265200 on May 31, 2001

J. Biol. Chem., Vol. 276, Issue 32, 30142-30149, August 10, 2001
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Overexpression of Macrophage Colony-stimulating Factor Receptor on Microglial Cells Induces an Inflammatory Response*

Olivera M. Mitrasinovic, Grace V. Perez, FeiFei Zhao, Yuen Ling LeeDagger , Clara Poon, and Greer M. Murphy Jr.§

From the Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305 and Dagger  Pathology Research, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304

Microglia are important in the inflammatory response in Alzheimer's disease (AD). We showed previously that macrophage colony-stimulating factor receptor (M-CSFR), encoded by the c-fms protooncogene, is overexpressed on microglia surrounding amyloid beta  (Abeta ) deposits in the APPV717F mouse model for AD. The M-CSFR is also increased on microglia after experimental brain injury and in AD. To determine the relevance of these findings, we transiently expressed M-CSFR on murine BV-2 and human SV-A3 microglial cell lines using an SV40-promoted c-fms construct. M-CSFR overexpression resulted in microglial proliferation and increased expression of inducible nitric-oxide synthase, the proinflammatory cytokines interleukin-1alpha , macrophage inflammatory protein 1-alpha , and interleukin-6 and of macrophage colony-stimulating factor (M-CSF) itself. Antibody neutralization of M-CSF showed that the M-CSFR-induced proinflammatory response was dependent on M-CSF in the culture media. By using a co-culture of c-fms-transfected murine microglia and rat organotypic hippocampal slices and a species-specific real time reverse transcriptase-polymerase chain reaction assay and enzyme-linked immunosorbent assay, we showed that M-CSFR overexpression on exogenous microglia induced expression of interleukin-1alpha by the organotypic culture. These results show that increased M-CSFR expression induces microglial proliferation, cytokine expression, and a paracrine inflammatory response, suggesting that in APPV717F mice increased M-CSFR on microglia could be an important factor in Abeta -induced inflammatory response.

* This work was supported by National Institute of Mental Health Grant MH57833 and the Alzheimer's Association.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: Neuroscience Research Laboratories, Dept. of Psychiatry and Behavioral Sciences, MSLS P-104, Stanford University School of Medicine, Stanford, CA 94305-5485. Tel.: 650-725-0565; Fax: 650-725-5714; E-mail: gmurphy@stanford.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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