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Molecular and Cellular Biology, November 2001, p. 7817-7825, Vol. 21, No. 22
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.22.7817-7825.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Mice with a Targeted Deletion of the Tetranectin Gene Exhibit a Spinal Deformity

Kousuke Iba,1,dagger Marian E. Durkin,1,Dagger Lise Johnsen,1,§ Ernst Hunziker,2 Karen Damgaard-Pedersen,3 Hong Zhang,1 Eva Engvall,4 Reidar Albrechtsen,1 and Ulla M. Wewer1,*

The Institute of Molecular Pathology, University of Copenhagen,1 and Department of Radiology, The Rigshospitalet University Hospital,3 Copenhagen, Denmark; The M. E. Muller Institute for Biomechanics, University of Bern, Bern, Switzerland2; and The Burnham Institute, La Jolla, California4

Received 25 June 2001/Returned for modification 3 August 2001/Accepted 22 August 2001

Tetranectin is a plasminogen-binding, homotrimeric protein belonging to the C-type lectin family of proteins. Tetranectin has been suggested to play a role in tissue remodeling, due to its ability to stimulate plasminogen activation and its expression in developing tissues such as developing bone and muscle. To test the functional role of tetranectin directly, we have generated mice with a targeted disruption of the gene. We report that the tetranectin-deficient mice exhibit kyphosis, a type of spinal deformity characterized by an increased curvature of the thoracic spine. The kyphotic angles were measured on radiographs. In 6-month-old normal mice (n = 27), the thoracic angle was 73° ± 2°, while in tetranectin-deficient 6-month-old mice (n = 35), it was 93° ± 2° (P < 0.0001). In approximately one-third of the mutant mice, X-ray analysis revealed structural changes in the morphology of the vertebrae. Histological analysis of the spines of these mice revealed an apparently asymmetric development of the growth plate and of the intervertebral disks of the vertebrae. In the most advanced cases, the growth plates appeared disorganized and irregular, with the disk material protruding through the growth plate. Tetranectin-null mice had a normal peak bone mass density and were not more susceptible to ovariectomy-induced osteoporosis than were their littermates as determined by dual-emission X-ray absorptiometry scanning. These results demonstrate that tetranectin plays a role in tissue growth and remodeling. The tetranectin-deficient mouse is the first mouse model that resembles common human kyphotic disorders, which affect up to 8% of the population.

* Corresponding author, Mailing address: Institute of Molecular Pathology, University of Copenhagen, Frederik V's vej 11, 2100 Copenhagen, Denmark. Phone: 45 35 32 60 56. Fax: 45 35 32 60 81. E-mail: ullaw{at}pai.ku.dk.

dagger Present address: Department of Orthopaedic Surgery, Monbetsu Hospital, Monbetsu, Japan.

Dagger Present address: National Cancer Institute, National Institutes of Health, Bethesda, Md.

§ Present address: Department of Anatomy and Neurobiology, University of Southern Denmark, Odense, Denmark.

Molecular and Cellular Biology, November 2001, p. 7817-7825, Vol. 21, No. 22
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.22.7817-7825.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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