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Ucma is not necessary for normal development of the mouse skeleton

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Bösl,  Michael R.
Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society;

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Citation

Eitzinger, N., Surmann-Schmitt, C., Bösl, M. R., Schett, G., Engelke, K., Hess, A., et al. (2012). Ucma is not necessary for normal development of the mouse skeleton. Bone, 50(3), 670-680. doi:10.1016/j.bone.2011.11.017.


Cite as: https://hdl.handle.net/11858/00-001M-0000-000F-8274-1
Abstract
Ucma (Upper zone of growth plate and Cartilage Matrix Associated
protein) is a highly conserved tyrosine-sulphated secreted protein of
Mw 17 kDa, which is expressed by juvenile chondrocytes.
To evaluate the physiological function of this novel cartilage protein,
we generated a Ucma-deficient mouse strain by introducing a
lacZ/neoR-cassette into the first exon of the Ucma gene. This mutation
results in the complete loss of Ucma mRNA and protein expression.
Surprisingly, however, although previous in vitro studies implied a
role for Ucma in calcification and ossification, these processes were
not affected in Ucma-deficient mice during normal development.
Likewise, cartilage development was normal. While in previous works
Ucma was mainly detected in the cartilage of embryonic and young mice,
we detected Ucma expression also in the adult cartilage of the ribs
using the lacZ cassette under the control of the Ucma promoter.
Moreover, Ucma protein was specifically detected in adult growth plate
cartilage by immunohistochemistry. Considering that skeletal
development in Ucma-deficient mice is not significantly impaired,
protein expression in adult cartilage indicates that Ucma might be
involved in skeletal homeostasis and in the mechanical properties of
the skeleton during challenging conditions such as ageing or disease.
(C) 2011 Elsevier Inc. All rights reserved.