ArticleIn vitro cellular & developmental biology. Animal2017
Proliferation of rabbit chondrocyte and inhibition of IL-1β-induced apoptosis through MEK/ERK signaling by statins.
Article in In vitro cellular & developmental biology. Animal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Deciduous pulp stem cell-derived extracellular vesicles stimulate the proliferation of cartilage progenitor cells via extracellular signal-regulated protein kinase 1/2 activation.Scientific reports · 2026Article
- Risk of metabolic abnormalities in osteoarthritis: a new perspective to understand its pathological mechanisms.Bone research · 2023Review
- Role of signal transduction pathways in IL-1β-induced apoptosis: Pathological and therapeutic aspects.Immunity, inflammation and disease · 2023Review
- Article
- 3D Printing for Bone-Cartilage Interface Regeneration.Frontiers in bioengineering and biotechnology · 2022Review
- Effect of high fat diet and excessive compressive mechanical force on pathologic changes of temporomandibular joint.Scientific reports · 2020Article
- Vitamin D3 protects articular cartilage by inhibiting the Wnt/β-catenin signaling pathway.Experimental and therapeutic medicine · 2020Article
- Plant homeodomain finger protein 23 inhibits autophagy and promotes apoptosis of chondrocytes in osteoarthritis.Chinese medical journal · 2019Article
- [Mechanical stress promotes cartilage repair in inflammatory environment].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Article
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Authors and funding
4 authors.
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Abstract
Chondrocyte plays a critical role in endochondral ossification and cartilage repair by maintaining the cartilaginous matrix. Statins have been widely used to lower the cholesterol level in patients with cardiovascular disorders. Previous research has demonstrated potential role of statins in chondrocyte proliferation. This study addresses the proliferation-regulatory effect of lovastatin in rabbit chondrocytes as well as the underlying signaling mechanisms, thereby exploring its potential application in chondrocyte-related disorders, such as cartilage damage and osteoarthritis. Rabbit chondrocytes were treated with lovastatin at multiple concentrations, and the proliferation rate was measured by CCK-8 test. The results showed significant increase in chondrocyte proliferation under lovastatin treatment. Using real-time quantitative PCR, it was observed that the expression levels of COL2A1, SOX-9, Caspase-3, and MMP-3 genes were significantly changed by lovastatin treatment. Western blotting analysis showed that the abundance of COL2A1, SOX-9, MEK1/2, p-MEK1/2, ERK1/2, p-ERK1/2, Caspase-3, and MMP-3 proteins was also significantly influenced by lovastatin treatment. Interleukine-1 beta (IL-1β) is involved in the progression of osteoarthritis (OA) by inducing articular cartilage and chondrocyte aging and senescence. In this study, we observed that lovastatin treatment inhibited IL-1β-induced chondrocyte apoptosis, while the combined treatment of lovastatin and U0126 evidently offset the apoptosis-inhibiting effect of lovastatin in chondrocyte proliferation. The expressional level and protein abundance of COL2A1, SOX-9, MEK1/2, p-MEK1/2, ERK1/2, p-ERK1/2, caspase-3, and MMP-3 genes showed significant alterations under the combined treatment. Together, our results suggested that lovastatin significantly promoted proliferation and inhibited the IL-1β-induced apoptosis in rabbit chondrocytes, which was mediated by the MEK/ERK signaling.
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