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Published online 14 January 2002. doi:10.1083/jcb.200111080
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© The Rockefeller University Press, 0021-9525/2002/1/227 $5.00
The Journal of Cell Biology, Volume 156, Number 2, January 21, 2002 227-232

Report

Bone abnormalities in latent TGF-ß binding protein (Ltbp)-3–null mice indicate a role for Ltbp-3 in modulating TGF-ß bioavailability



Branka Dabovic1, Yan Chen1, Cristina Colarossi1, Hiroto Obata1, Laura Zambuto1, Mary Ann Perle2 and Daniel B. Rifkin1,3

1 Department of Cell Biology, New York University School of Medicine, New York, NY 10016
2 Department of Pathology, New York University School of Medicine, New York, NY 10016
3 Department of Medicine, New York University School of Medicine, New York, NY 10016

Address correspondence to B. Dabovic, Dept. of Cell Biology, New York University Medical School, 550 First Ave., New York, NY 10016. Tel.: (212) 263-5327. Fax: (212) 263-0595. E-mail: dabovb01{at}med.nyu.edu

The TGF-ßs are multifunctional proteins whose activities are believed to be controlled by interaction with the latent TGF-ß binding proteins (LTBPs). In spite of substantial effort, the precise in vivo significance of this interaction remains unknown. To examine the role of the Ltbp-3, we made an Ltbp-3–null mutation in the mouse by gene targeting. Homozygous mutant animals develop cranio-facial malformations by day 10. At 2 mo, there is a pronounced rounding of the cranial vault, extension of the mandible beyond the maxilla, and kyphosis. Histological examination of the skulls from null animals revealed ossification of the synchondroses within 2 wk of birth, in contrast to the wild-type synchondroses, which never ossify. Between 6 and 9 mo of age, mutant animals also develop osteosclerosis and osteoarthritis. The pathological changes of the Ltbp-3–null mice are consistent with perturbed TGF-ß signaling in the skull and long bones. These observations give support to the notion that LTBP-3 is important for the control of TGF-ß action. Moreover, the results provide the first in vivo indication for a role of LTBP in modulating TGF-ß bioavailability.

Key Words: latent TGF-ß binding protein; TGF-ß; osteoarthritis; osteosclerosis; synchondroses


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