Comprehensive profiling analysis of actively resorbing osteoclasts identifies critical signaling pathways regulated by bone substrate

Files

hdl_94187.pdf (1.45 MB)
  (Published version)

Date

2014

Authors

Purdue, P.
Crotti, T.
Shen, Z.
Swantek, J.
Li, J.
Hill, J.
Hanidu, A.
Dimock, J.
Nabozny, G.
Goldring, S.

Editors

Advisors

Journal Title

Journal ISSN

Volume Title

Type:

Journal article

Citation

Scientific Reports, 2014; 4(1):7595-1-7595-11

Statement of Responsibility

P. Edward Purdue, Tania N. Crotti, Zhenxin Shen, Jennifer Swantek, Jun Li, Jonathan Hill, Adedayo Hanidu, Janice Dimock, Gerald Nabozny, Steven R. Goldring, Kevin P. McHugh

Conference Name

Abstract

As the only cells capable of efficiently resorbing bone, osteoclasts are central mediators of both normal bone remodeling and pathologies associates with excessive bone resorption. However, despite the clear evidence of interplay between osteoclasts and the bone surface in vivo, the role of the bone substrate in regulating osteoclast differentiation and activation at a molecular level has not been fully defined. Here, we present the first comprehensive expression profiles of osteoclasts differentiated on authentic resorbable bone substrates. This analysis has identified numerous critical pathways coordinately regulated by osteoclastogenic cytokines and bone substrate, including the transition from proliferation to differentiation, and sphingosine-1-phosphate signaling. Whilst, as expected, much of this program is dependent upon integrin beta 3, the pre-eminent mediator of osteoclast-bone interaction, a surprisingly significant portion of the bone substrate regulated expression signature is independent of this receptor. Together, these findings identify an important hitherto underappreciated role for bone substrate in osteoclastogenesis.

School/Discipline

Dissertation Note

Provenance

Description

Access Status

Rights

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

License

Grant ID

Call number

Persistent link to this record