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Molecular and Cellular Biology, March 2002, p. 1438-1445, Vol. 22, No. 5
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.5.1438-1445.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Ultrastructural Cartilage Abnormalities in MIA/CD-RAP-Deficient Mice

Markus Moser,1 Anja-Katrin Bosserhoff,1 Ernst B. Hunziker,2 Linda Sandell,3 Reinhard Fässler,4 and Reinhard Buettner5*

Institute of Pathology, University Hospital RWTH, D-52074 Aachen,1 Institute of Pathology, University of Bonn, D-53127 Bonn, Germany,5 M. E. Müller-Institut for Biomechanics, University of Bern, CH-010 Bern, Switzerland,2 Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri 63110,3 Department of Experimental Pathology, Lund University, S-22185 Lund, Sweden4

Received 31 July 2001/ Returned for modification 31 August 2001/ Accepted 19 November 2001

MIA/CD-RAP is a small, soluble protein secreted from malignant melanoma cells and from chondrocytes. Recent evidence has identified MIA/CD-RAP as the prototype of a small family of extracellular proteins adopting an SH3 domain-like fold. It is thought that interaction between MIA/CD-RAP and specific epitopes in extracellular matrix proteins regulates the attachment of tumor cells and chondrocytes. In order to study the consequences of MIA/CD-RAP deficiency in vivo, we generated mice with a targeted gene disruption. The complete absence of MIA/CD-RAP mRNA and protein expression was demonstrated by reverse transcriptase, Western blot analysis, and enzyme-linked immunosorbent assay measurements of whole-embryo extracts. MIA-/- mice were viable and developed normally, and histological examination of the organs by means of light microscopy revealed no major abnormalities. In contrast, electron microscopic studies of cartilage composition revealed subtle defects in collagen fiber density, diameter, and arrangement, as well as changes in the number and morphology of chondrocytic microvilli. Taken together, our data indicate that MIA/CD-RAP is essentially required for formation of the highly ordered ultrastructural fiber architecture in cartilage and may have a role in regulating chondrocyte matrix interactions.

* Corresponding author. Mailing address: Institut für Pathologie, Universitätsklinikum Bonn, Sigmund-Freud-Str. 25, D-53127 Bonn, Germany. Phone: (49) 228-287-5377. Fax: (49) 228-287-5030. E-mail: Reinhard.Buettner{at}ukb.uni-bonn.de.

Molecular and Cellular Biology, March 2002, p. 1438-1445, Vol. 22, No. 5
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.5.1438-1445.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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