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Updated: Mar 23, 2026
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice by inhibiting Sik3
Yasuhito Yahara1,2, Hiroshi Takemori3, Minoru Okada1
1Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application, Kyoto University, 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Abstract:
Osteoarthritis is a common debilitating joint disorder. Risk factors for osteoarthritis include age, which is associated with thinning of articular cartilage. Here we generate chondrocyte-specific salt-inducible kinase 3 (Sik3) conditional knockout mice that are resistant to osteoarthritis with thickened articular cartilage owing to a larger chondrocyte population. We also identify an edible Pteridium aquilinum compound, pterosin B, as a Sik3 pathway inhibitor. We show that either Sik3 deletion or intraarticular injection of mice with pterosin B inhibits chondrocyte hypertrophy and protects cartilage from osteoarthritis. Collectively, our results suggest Sik3 regulates the homeostasis of articular cartilage and is a target for the treatment of osteoarthritis, with pterosin B as a candidate therapeutic.
Insights
Researchers identified salt-inducible kinase 3 (Sik3) as a key regulator of articular cartilage. Inhibiting Sik3 or using pterosin B protected mice from osteoarthritis, suggesting new therapeutic targets.
Area of Science:
- Biomedical Science
- Orthopedics
- Molecular Biology
Background:
- Osteoarthritis is a prevalent joint disorder linked to aging and articular cartilage thinning.
- Understanding the molecular mechanisms regulating cartilage homeostasis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of salt-inducible kinase 3 (Sik3) in articular cartilage maintenance.
- To identify potential therapeutic strategies for osteoarthritis targeting the Sik3 pathway.
Main Methods:
- Generation of chondrocyte-specific Sik3 conditional knockout mice.
- Administration of pterosin B, a Pteridium aquilinum compound, to mice.
- Assessment of articular cartilage thickness, chondrocyte population, and hypertrophy.
Main Results:
- Sik3 knockout mice exhibited thickened articular cartilage and resistance to osteoarthritis.
- Pterosin B inhibited chondrocyte hypertrophy and protected cartilage from osteoarthritis.
- Sik3 deletion or pterosin B treatment led to a larger chondrocyte population.
Conclusions:
- Sik3 plays a critical role in regulating articular cartilage homeostasis.
- Targeting Sik3, potentially with pterosin B, offers a promising therapeutic avenue for osteoarthritis treatment.
