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Conditional deletion of E11/Podoplanin in bone protects against ovariectomy-induced increases in osteoclast formation and activity

Staines, Katherine; Hopkinson, Mark; Dillon, Scott; Stephen, Louise; Fleming, Robert; Sophocleous, Antonia; Buttle, David; Pitsillides, Andrew; Farquharson, Colin

Authors

Katherine Staines

Mark Hopkinson

Scott Dillon

Louise Stephen

Robert Fleming

Antonia Sophocleous

David Buttle

Andrew Pitsillides

Colin Farquharson



Abstract

E11/Podoplanin (Pdpn) is implicated in early osteocytogenesis and the formation of osteocyte dendrites. This dendritic network is critical for bone modeling/remodeling, through the production of the receptor for receptor activator of nuclear factor κB (RANK)-ligand (RANKL). Despite this, the role of Pdpn in the control of bone remodeling is yet to be established in vivo. Here we utilised bone-specific Pdpn conditional knockout mice (cKO) to examine the role of Pdpn in the bone loss associated with ovariectomy (OVX). MicroCT revealed that Pdpn deletion had no significant effect on OVX-induced changes in trabecular microarchitecture. Significant differences between genotypes were observed in the trabecular pattern factor (P

Journal Article Type Article
Acceptance Date Dec 23, 2019
Publication Date Jan 10, 2020
Deposit Date Jan 2, 2020
Publicly Available Date Jan 6, 2020
Print ISSN 0144-8463
Electronic ISSN 1573-4935
Publisher Portland Press
Peer Reviewed Peer Reviewed
Volume 40
Issue 1
DOI https://doi.org/10.1042/BSR20190329
Keywords bone, E11/podoplanin, osteoclast, osteocyte, osteoporosis
Public URL http://researchrepository.napier.ac.uk/Output/2442586

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Conditional Deletion Of E11/Podoplanin In Bone Protects Against Ovariectomy-induced Increases In Osteoclast Formation And Activity (1.3 Mb)
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Publisher Licence URL
http://creativecommons.org/licenses/by/4.0/

Copyright Statement
© 2020 The Author(s). This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution
License 4.0 (CC BY).





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