Nuclear factor erythroid 2-related factor 2 (Nrf2) deficiency causes age-dependent progression of female osteoporosis.


Journal

BMC musculoskeletal disorders
ISSN: 1471-2474
Titre abrégé: BMC Musculoskelet Disord
Pays: England
ID NLM: 100968565

Informations de publication

Date de publication:
25 Nov 2022
Historique:
received: 20 08 2022
accepted: 02 11 2022
entrez: 26 11 2022
pubmed: 27 11 2022
medline: 30 11 2022
Statut: epublish

Résumé

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor for cellular redox homeostasis. The association of Nrf2 with elderly female osteoporotic has yet to be fully described. The aim was to elucidate a potential age-dependent Nrf2 contribution to female osteoporosis in mice. Eighteen female wild type (WT) and 16 Nrf2-knockout (KO) mice were sacrificed at different ages (12 weeks = young mature adult and 90 weeks = old) to analyze their femurs. The morphological properties (trabecular and cortical) were evaluated by micro-computed tomography (μCT) and compared to gold standard histochemistry analysis. The quasi-static compression tests were performed to calculate the mechanical properties of bones. Additionally, the population of bone resorbing cells and aromatase expression by osteocytes was immunohistochemically evaluated and empty osteocyte lacunae was counted in cortical bone. Old Nrf2-KO mice revealed a significantly reduced trabecular bone mineral density (BMD), cortical thickness, cortical area, and bone fraction compared to old WT mice, regardless of no significant difference in skeletally mature young adult mice between WT and KO. Specifically, while all old WT mice showed thin metaphyseal trabeculae, trabecular bone was completely absent in 60% of old KO mice. Additionally, old KO mice showed significantly more osteoclast-like cells and fewer aromatase-positive osteocytes than WT mice, whereas the occurrence of empty osteocyte lacunae did not differ between both groups. Nrf2-KO mice further showed an age-dependently reduced fracture resilience compared to age-matched WT mice. Our results suggest that chronic Nrf2 loss can lead to age-dependent progression of female osteoporosis.

Sections du résumé

BACKGROUND BACKGROUND
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor for cellular redox homeostasis. The association of Nrf2 with elderly female osteoporotic has yet to be fully described. The aim was to elucidate a potential age-dependent Nrf2 contribution to female osteoporosis in mice.
METHODS METHODS
Eighteen female wild type (WT) and 16 Nrf2-knockout (KO) mice were sacrificed at different ages (12 weeks = young mature adult and 90 weeks = old) to analyze their femurs. The morphological properties (trabecular and cortical) were evaluated by micro-computed tomography (μCT) and compared to gold standard histochemistry analysis. The quasi-static compression tests were performed to calculate the mechanical properties of bones. Additionally, the population of bone resorbing cells and aromatase expression by osteocytes was immunohistochemically evaluated and empty osteocyte lacunae was counted in cortical bone.
RESULTS RESULTS
Old Nrf2-KO mice revealed a significantly reduced trabecular bone mineral density (BMD), cortical thickness, cortical area, and bone fraction compared to old WT mice, regardless of no significant difference in skeletally mature young adult mice between WT and KO. Specifically, while all old WT mice showed thin metaphyseal trabeculae, trabecular bone was completely absent in 60% of old KO mice. Additionally, old KO mice showed significantly more osteoclast-like cells and fewer aromatase-positive osteocytes than WT mice, whereas the occurrence of empty osteocyte lacunae did not differ between both groups. Nrf2-KO mice further showed an age-dependently reduced fracture resilience compared to age-matched WT mice.
CONCLUSION CONCLUSIONS
Our results suggest that chronic Nrf2 loss can lead to age-dependent progression of female osteoporosis.

Identifiants

pubmed: 36434613
doi: 10.1186/s12891-022-05942-1
pii: 10.1186/s12891-022-05942-1
pmc: PMC9700883
doi:

Substances chimiques

NF-E2-Related Factor 2 0
Aromatase EC 1.14.14.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1015

Informations de copyright

© 2022. The Author(s).

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Auteurs

Yusuke Kubo (Y)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany. ykubo@ukaachen.de.

Jesus Abraham Herrera Gonzalez (JAH)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Rainer Beckmann (R)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Marek Weiler (M)

Institute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.

Helda Pahlavani (H)

Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.

Mauricio Cruz Saldivar (MC)

Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.

Katharina Szymanski (K)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Stefanie Rosenhain (S)

Institute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.

Athanassios Fragoulis (A)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Sander Leeflang (S)

Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.

Alexander Slowik (A)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Felix Gremse (F)

Institute for Experimental Molecular Imaging, Helmholtz Institute for Biomedical Engineering, Uniklinik RWTH Aachen, Forckenbeckstraße 55, 52074, Aachen, Germany.

Michael Wolf (M)

Department of Orthodontics, Uniklinik RWTH Aachen, Pauwelsstraße 30, 52074, Aachen, Germany.

Mohammad Javad Mirzaali (MJ)

Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.

Amir Abbas Zadpoor (AA)

Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology (TU Delft), Mekelweg 2, 2628, CD, Delft, The Netherlands.

Christoph Jan Wruck (CJ)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Thomas Pufe (T)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Mersedeh Tohidnezhad (M)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.

Holger Jahr (H)

Department of Anatomy and Cell Biology, Uniklinik RWTH Aachen, Wendlingweg 2, 52074, Aachen, Germany.
Institute of Structural Mechanics and Lightweight Design, RWTH Aachen University, Wüllnerstraße 7, 52062, Aachen, Germany.

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