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Ucma is not necessary for normal development of the mouse skeleton

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Boesl,  M.
Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society;

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Citation

Eitzinger, N., Surmann-Schmitt, C., Boesl, M., 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: http://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.