RANKL-Induced Increase in Cathepsin K Levels Restricts Cortical Expansion in a Periostin-Dependent Fashion: A Potential New Mechanism of Bone Fragility.
AGING
ANTIRESORPTIVES
GENETIC ANIMAL MODELS
NON-COLLAGENOUS PROTEIN
OSTEOPOROSIS
Journal
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
ISSN: 1523-4681
Titre abrégé: J Bone Miner Res
Pays: United States
ID NLM: 8610640
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
revised:
26
03
2021
received:
30
06
2020
accepted:
08
04
2021
pubmed:
16
4
2021
medline:
10
8
2021
entrez:
15
4
2021
Statut:
ppublish
Résumé
Receptor activator of nuclear factor-κΒ ligand (RANKL) is necessary and sufficient to promote osteoclastogenesis and a key pathogenic factor in osteoporosis. Failure of periosteal apposition to compensate for bone loss due to endosteal resorption further contributes to bone fragility. Whether these two processes are biologically related, however, remains unknown. Using high-resolution peripheral quantitative computed tomography (HR-pQCT), we first examined cortical bone parameters at distal radius and tibia in postmenopausal women (PMW) as well as in cadaveric human adult humeri. Increases in medullary area were negatively correlated with cortical bone volume but positively with total bone volume, and this relationship was stronger in the dominant arm, suggesting a mechanically driven process. To investigate the role of RANKL in this dual process, we used mice overexpressing huRANKL (huRANKLTg
Substances chimiques
Ligands
0
Cathepsin K
EC 3.4.22.38
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1636-1645Informations de copyright
© 2021 American Society for Bone and Mineral Research (ASBMR).
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