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Characterization of bone morphology in CCN5/WISP5 knockout mice

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Journal of Cell Communication and Signaling Aims and scope

A Correction to this article was published on 17 February 2018

This article has been updated

Abstract

CCN5/WISP2 is part of the CCN family of matricellular proteins, but is distinct in that it lacks the C-terminal (CT) domain. Although CCN5 has been shown to impact cell proliferation and differentiation in vitro, its role in vivo is unclear. We therefore generated mice using ES cells developed by the Knockout Mouse Project (KOMP) in which exons 2-5, which encode the all of the conserved protein coding regions, are replaced by a lacZ cassette. Ccn5LacZ/LacZ mice were viable and apparently normal. Based on previous studies showing that CCN5 impacts osteoblast proliferation and differentiation, we performed an analysis of adult bone phenotype. LacZ expression was examined in adult bone, and was found to be strong within the periosteum, but not in trabecular bone or bone marrow. Micro-CT analysis revealed no apparent changes in bone mineral density (BMD) or bone tissue volume (BV/TV) in Ccn5LacZ/LacZ mice. These studies indicate that CCN5 is not required for normal bone formation, but they do not rule out a role in mechanotransduction or repair processes. The availability of Ccn5LacZ mice enables studies of CCN5 expression and function in multiple tissues.

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Change history

  • 17 February 2018

    In the original publication’s title CCN5/WISP5 should have been CCN5/WISP2.

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Acknowledgements

This work was supported by NIAMS/NIH grants R01 AR052686 and R21 AR071734 to KML.

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Correspondence to Karen M. Lyons.

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Jie Jiang and Gexin Zhao are co first authors

An erratum to this article is available at https://doi.org/10.1007/s12079-018-0463-5.

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Jiang, J., Zhao, G. & Lyons, K.M. Characterization of bone morphology in CCN5/WISP5 knockout mice. J. Cell Commun. Signal. 12, 265–270 (2018). https://doi.org/10.1007/s12079-018-0457-3

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  • DOI: https://doi.org/10.1007/s12079-018-0457-3

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