Differential expression of the inflammatory ciita gene may be accompanied by altered bone properties in intact sex steroid-deficient female rats.

BMD Biomechanical testing Bone Ciita Inflammation Ovariectomy Rat micro-CT

Journal

BMC research notes
ISSN: 1756-0500
Titre abrégé: BMC Res Notes
Pays: England
ID NLM: 101462768

Informations de publication

Date de publication:
19 Dec 2023
Historique:
received: 12 04 2023
accepted: 28 09 2023
medline: 20 12 2023
pubmed: 20 12 2023
entrez: 20 12 2023
Statut: epublish

Résumé

The class II transactivator (CIITA), encoded by the CIITA gene, controls expression of immune response regulators, which affect bone homeostasis. Previously, we investigated a functional CIITA polymorphism in elderly women. Women carrying the allele associated with lower CIITA levels displayed higher bone mineral density (BMD), but also higher bone loss. The present exploratory study in a rat model sought to investigate effects of differential expression of Ciita on bone structural integrity and strength. Two strains DA (normal-to-high expression) and DA.VRA4 (lower expression) underwent ovariectomy (OVX) or sham-surgery at ~ 14-weeks of age (DA OVX n = 8, sham n = 4; DA.VRA4 OVX n = 10, sham n = 2). After 16-weeks, femoral BMD and bone mineral content (BMC) were measured and morphometry and biomechanical testing performed. In DA.VRA4 rats, BMD/BMC, cross-sectional area and biomechanical properties were lower. Ciita expression was accompanied by OVX-induced changes to cross-sectional area and femoral shaft strength; DA rats had lower maximum load-to-fracture. Thus, while lower Ciita expression associated with lower bone mass, OVX induced changes to structural and mechanical bone properties were less pronounced. The data tentatively suggests association between Ciita expression and structural and mechanical bone properties, and a possible role in bone changes resulting from estrogen deficiency.

Identifiants

pubmed: 38115045
doi: 10.1186/s13104-023-06543-4
pii: 10.1186/s13104-023-06543-4
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

372

Informations de copyright

© 2023. The Author(s).

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Auteurs

Vivi Fh Jensen (VF)

Department of Clinical Sciences Malmö, Clinical and Molecular Osteoporosis Research Unit, Lund University, Malmö, 214 28, Sweden.
Department of Orthopaedics, Skåne University Hospital, Malmö, 205 02, Sweden.

Maria Swanberg (M)

Department of Clinical Sciences Malmö, Clinical and Molecular Osteoporosis Research Unit, Lund University, Malmö, 214 28, Sweden.
Department of Experimental Medical Science, Translational Neurogenetics Unit, Lund University, Lund, 221 84, Sweden.

Maria Herlin (M)

Department of Clinical Sciences Malmö, Clinical and Molecular Osteoporosis Research Unit, Lund University, Malmö, 214 28, Sweden.
Department of Orthopaedics, Skåne University Hospital, Malmö, 205 02, Sweden.

Fiona E McGuigan (FE)

Department of Clinical Sciences Malmö, Clinical and Molecular Osteoporosis Research Unit, Lund University, Malmö, 214 28, Sweden. fiona.mcguigan@med.lu.se.
Department of Orthopaedics, Skåne University Hospital, Malmö, 205 02, Sweden. fiona.mcguigan@med.lu.se.

Niklas R Jørgensen (NR)

Department of Clinical Biochemistry, Centre of Diagnostic Investigation, Rigshospitalet, Glostrup, 2600, Denmark.
Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, 2200, Denmark.

Kristina E Akesson (KE)

Department of Clinical Sciences Malmö, Clinical and Molecular Osteoporosis Research Unit, Lund University, Malmö, 214 28, Sweden.
Department of Orthopaedics, Skåne University Hospital, Malmö, 205 02, Sweden.

Classifications MeSH