CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing.
CTRP3
bone
fracture healing
nonunion
regeneration
Journal
Journal of orthopaedic research : official publication of the Orthopaedic Research Society
ISSN: 1554-527X
Titre abrégé: J Orthop Res
Pays: United States
ID NLM: 8404726
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
11
10
2019
accepted:
24
11
2019
pubmed:
7
12
2019
medline:
14
8
2020
entrez:
7
12
2019
Statut:
ppublish
Résumé
C1q/TNF-related protein 3 (CTRP3) is a cytokine known to regulate a variety of metabolic processes. Though previously undescribed in the context of bone regeneration, high throughput gene expression experiments in mice identified CTRP3 as one of the most highly upregulated genes in fracture callus tissue. Hypothesizing a positive regulatory role for CTRP3 in bone regeneration, we phenotyped skeletal development and fracture healing in CTRP3 knockout (KO) and CTRP3 overexpressing transgenic (TG) mice relative to wild-type (WT) control animals. CTRP3 KO mice experienced delayed endochondral fracture healing, resulting in abnormal mineral distribution, the presence of periosteal marrow compartments, and a nonunion-like state. Decreased osteoclast number was also observed in CTRP3 KO mice, whereas CTRP3 TG mice underwent accelerated callus remodeling. Gene expression profiling revealed a broad impact on osteoblast/osteoclast lineage commitment and metabolism, including arrested progression toward mature skeletal lineages in the KO group. A single systemic injection of CTRP3 protein at the time of fracture was insufficient to phenocopy the chronic TG healing response in WT mice. By associating CTRP3 levels with fracture healing progression, these data identify a novel protein family with potential therapeutic and diagnostic value. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:00-19966, 2020.
Identifiants
pubmed: 31808575
doi: 10.1002/jor.24553
pmc: PMC7162724
mid: NIHMS1064760
doi:
Substances chimiques
Adipokines
0
CORS26 protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
996-1006Subventions
Organisme : NIDCR NIH HHS
ID : F32 DE026346
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007445
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR055607
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR069620
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK084171
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR066028
Pays : United States
Organisme : NIAMS NIH HHS
ID : F30 AR071201
Pays : United States
Informations de copyright
© 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
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