A loss of primary cilia by a reduction in mTOR signaling correlates with age-related deteriorations in condylar cartilage.
Aging
Chondrocyte
Condylar cartilage
Primary cilia
Temporomandibular joint-osteoarthritis
mTOR
Journal
GeroScience
ISSN: 2509-2723
Titre abrégé: Geroscience
Pays: Switzerland
ID NLM: 101686284
Informations de publication
Date de publication:
25 Mar 2024
25 Mar 2024
Historique:
received:
01
11
2023
accepted:
16
03
2024
medline:
25
3
2024
pubmed:
25
3
2024
entrez:
25
3
2024
Statut:
aheadofprint
Résumé
Age-related deterioration of condylar cartilage is an etiological factor in temporomandibular joint-osteoarthritis (TMJ-OA). However, its underlying mechanism remains unknown. Therefore, we examined age-related changes and the relationship between mTOR signaling and primary cilia in condylar cartilage to determine the intrinsic mechanisms of age-related TMJ-OA. Age-related morphological changes were analyzed using micro-computed tomography and safranin O-stained histological samples of the mandibular condyle of C57BL/6J mice (up to 78 weeks old). Immunohistochemistry was used to assess the activity of mTOR signaling, primary cilia frequency, and Golgi size of condylar chondrocytes. Four-week-old mice receiving an 11-week series of intraperitoneal injections of rapamycin, a potent mTOR signaling inhibitor, were used for the histological evaluation of the condylar cartilage. The condylar cartilage demonstrated an age-related reduction in cartilage area, including chondrocyte size, cell density, and cell size distribution. The Golgi size, primary cilia frequency, and mTOR signaling also decreased with age. Rapamycin injections resulted in both diminished cartilage area and cell size, resembling the phenotypes observed in aged mice. Rapamycin-injected mice also exhibited a smaller Golgi size and lower primary cilia frequency in condylar cartilage. We demonstrated that a loss of primary cilia due to a decline in mTOR signaling was correlated with age-related deteriorations in condylar cartilage. Our findings provide new insights into the tissue homeostasis of condylar cartilage, contributing to understanding the etiology of age-related TMJ-OA.
Identifiants
pubmed: 38526843
doi: 10.1007/s11357-024-01143-x
pii: 10.1007/s11357-024-01143-x
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Society for the Promotion of Science
ID : JP19K19088
Organisme : Japan Society for the Promotion of Science
ID : JP21K17035
Informations de copyright
© 2024. The Author(s), under exclusive licence to American Aging Association.
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