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CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage
Miho Kuwahara1,2, Koichi Kadoya3, Sei Kondo1
1Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8525, Japan.
International Journal of Molecular Sciences
|October 17, 2020
Summary
Aging accelerates osteoarthritis by damaging cartilage. CCN3 protein accumulation in chondrocytes is linked to aging and promotes senescence, potentially driving cartilage degeneration via p53 and p21 pathways.
Area of Science:
- Biogerontology
- Cartilage Biology
- Molecular Biology
Background:
- Aging is a primary risk factor for osteoarthritis, a condition marked by articular cartilage degeneration.
- CCN3, a CCN family member, plays roles in chondrocyte development, differentiation, and regeneration.
Purpose of the Study:
- To investigate the role of CCN3 in cartilage maintenance during aging.
- To determine if CCN3 contributes to chondrocyte senescence and osteoarthritis pathogenesis.
Main Methods:
- Analyzed CCN3 expression in aging mouse chondrocytes and human articular chondrocytes.
- Utilized in vitro models (human chondrocytes, RCS cells) with induced senescence (H2O2).
- Generated cartilage-specific CCN3-overexpressing transgenic mice.
Main Results:
- CCN3 expression increased with age and correlated with p21 and p53 in mouse chondrocytes.
- CCN3 overexpression enhanced chondrocyte senescence markers (p21, p53, SA-β-gal) in vitro.
- Transgenic mice exhibited rapid knee joint degeneration and inflammation, mirroring human chondrocyte findings.
Conclusions:
- CCN3 serves as a novel chondrocyte senescence marker.
- CCN3 overexpression in cartilage can promote chondrocyte senescence, contributing to articular cartilage degeneration through p53 and p21 induction.
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