Death Receptor 3 (TNFRSF25) Increases mineral apposition by osteoblasts and region specific new bone formation in the axial skeleton of male DBA/1 mice

Collins, Fraser L., Williams, Jessica, Bloom, Anja C., Stone, Michael D., Choy, Ernest Ho Sing ORCID: https://orcid.org/0000-0003-4459-8609, Wang, Edward Chung Yern ORCID: https://orcid.org/0000-0002-2243-4964 and Williams, Anwen Sian 2015. Death Receptor 3 (TNFRSF25) Increases mineral apposition by osteoblasts and region specific new bone formation in the axial skeleton of male DBA/1 mice. Journal of Immunology Research 2015 , -. 10.1155/2015/901679

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Abstract

Objectives. Genome wide association studies identified TNFSF member TNF-like protein 1A (TL1A, TNFSF15) as a potential modulator of ankylosing spondylitis (AS). TL1A is the only confirmed TNFSF ligand of death receptor 3 (DR3, TNFRSF25); however, its role in disease pathology is not characterised. We evaluated DR3’s role in controlling osteoblast- (OB-) dependent bone formation in vitro and in vivo. Methods. Osteoprogenitor cells and OB were cultured from male DR3-deficient () and wild-type () DBA/1 mice. DR3 and RANKL expression were tested by flow cytometry. Alkaline phosphatase and mineralization were quantified. Osteopontin, osteoprotegerin, and pro MMP-9 were measured by ELISA. A fluorescent probe (BoneTag) was used to measure in vivo mineralization in 10-month-old mice. Results. DR3 was expressed on osteoprogenitors and OB from mice. Alkaline phosphatase, osteopontin, and mineral apposition were significantly elevated in cultures. Levels of RANKL were comparable whilst osteoprotegerin was significantly increased in cultures. In vivo incorporation of BoneTag was significantly lower in the thoracic vertebrae of 10-month-old mice. Conclusions. These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition. They potentially begin to explain the atypical pattern of new bone formation observed in the axial skeleton of grouped, aging DBA/1 mice.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Medicine Systems Immunity Research Institute (SIURI)
Subjects:	R Medicine > R Medicine (General)
Additional Information:	Article ID 901679, 9 pages
Publisher:	Hindawi Publishing Corporation
ISSN:	2314-8861
Funders:	Arthritis Research UK
Date of First Compliant Deposit:	30 March 2016
Date of Acceptance:	1 December 2014
Last Modified:	05 May 2023 18:14
URI:	https://orca.cardiff.ac.uk/id/eprint/69661

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