Sirtuin 3 deficiency does not impede digit regeneration in mice.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
11 11 2019
11 11 2019
Historique:
received:
08
02
2019
accepted:
25
10
2019
entrez:
13
11
2019
pubmed:
13
11
2019
medline:
5
11
2020
Statut:
epublish
Résumé
The mitochondrial deacetylase sirtuin 3 (SIRT3) is thought to be one of the main contributors to metabolic flexibility-promoting mitochondrial energy production and maintaining homeostasis. In bone, metabolic profiles are tightly regulated and the loss of SIRT3 has deleterious effects on bone volume in vivo and on osteoblast differentiation in vitro. Despite the prominent role of this protein in bone stem cell proliferation, metabolic activity, and differentiation, the importance of SIRT3 for regeneration after bone injury has never been reported. We show here, using the mouse digit amputation model, that SIRT3 deficiency has no impact on the regenerative capacity and architecture of bone and soft tissue. Regeneration occurs in SIRT3 deficient mice in spite of the reduced oxidative metabolic profile of the periosteal cells. These data suggest that bone regeneration, in contrast to homeostatic bone turnover, is not reliant upon active SIRT3, and our results highlight the need to examine known roles of SIRT3 in the context of injury.
Identifiants
pubmed: 31712596
doi: 10.1038/s41598-019-52921-z
pii: 10.1038/s41598-019-52921-z
pmc: PMC6848098
doi:
Substances chimiques
Biomarkers
0
Sirtuin 3
EC 3.5.1.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
16491Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM103629
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM121301
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM104940
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM115516
Pays : United States
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