ArticleMolecular medicine reports2017
Beclin 1 overexpression inhibits chondrocyte apoptosis and downregulates extracellular matrix metabolism in osteoarthritis.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 38 citations in OpenAlex.
- Meckel's cartilage midsegment: spatiotemporal dynamics and osteogenic role in mice.Cell and tissue research · 2026Article
- Modulating Autophagy in Osteoarthritis: Exploring Emerging Therapeutic Drug Targets.International journal of molecular sciences · 2024Review
- New insights into the mechanisms and therapeutic strategies of chondrocyte autophagy in osteoarthritis.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Review
- Spatial and chronological localization of septoclasts in the mouse Meckel's cartilage.Histochemistry and cell biology · 2022Article
- Senescent skeletal cells cross-talk with synovial cells plays a key role in the pathogenesis of osteoarthritis.Arthritis research & therapy · 2022Review
- Data Integration Reveals the Potential Biomarkers of Circulating MicroRNAs in Osteoarthritis.Diagnostics (Basel, Switzerland) · 2021Review
- Influence of swimming exercise on the expression of apoptotic gene caspase-3 in chondrocytes in osteoarthritis.American journal of translational research · 2021Article
- Recombinant human gelsolin promotes the migration of human articular cartilage chondrocytes by regulating gene expressionOsteoarthritis and cartilage open · 2020Article
- Diverse Fate of an Enigmatic Structure: 200 Years of Meckel's Cartilage.Frontiers in cell and developmental biology · 2020Review
- Article
- Catalpol Attenuates IL-1β Induced Matrix Catabolism, Apoptosis and Inflammation in Rat Chondrocytes and Inhibits Cartilage Degeneration.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- β1,4-galactosyltransferase-I protects chondrocytes against TNF-induced apoptosis by blocking the TLR4 signaling pathway.American journal of translational research · 2019Article
- Modulated Autophagy by MicroRNAs in Osteoarthritis Chondrocytes.BioMed research international · 2019Review
- The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review.BioMed research international · 2019Review
- 29-kDa FN-f inhibited autophagy through modulating localization of HMGB1 in human articular chondrocytes.BMB reports · 2018Article
- MicroRNAs and Osteoarthritis.Cells · 2018Review
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In the present study, the expression of Beclin 1 in osteoarthritis (OA) cartilage tissue was investigated, and also its role in proliferation, apoptosis and expression of matrix metalloproteinases (MMPs) in chondrocytes obtained from patients with OA. Beclin 1 expression in cartilage tissue from OA patients, and in the age- and sex-matched controls, was detected by immunohistochemistry, semi-quantitative polymerase chain reaction and western blotting. Chondrocytes were divided into control and Beclin 1-overexpressed groups. After transfection for 48, 72 and 96 h, cell viability, apoptosis, the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway and MMPs were examined. The mRNA and protein expression levels of Beclin 1 were significantly decreased in cartilage tissue from OA patients compared with the sex- and age-matched controls (P<0.05). In chondrocytes from OA patients, Beclin 1 overexpression significantly increased cell viability (P<0.05). Beclin 1 overexpression additionally decreased the degree of apoptosis, as demonstrated by Hoechst staining and flow cytometric analysis. B-cell lymphoma-2 (Bcl-2) was upregulated, and Bcl-2 associated X was downregulated, following Beclin 1 overexpression (P<0.05). The PI3K/Akt/mTOR signaling pathway was mitigated following Beclin 1 overexpression (P<0.05). In addition, MMP1, MMP3 and MMP13 were downregulated after Beclin 1 overexpression (P<0.05). Taken together, low expression levels of Beclin 1 may contribute towards the degeneration of chondrocytes. Beclin 1 overexpression increased cell viability, inhibited apoptosis and MMPs, likely via the PI3K/Akt/mTOR signaling pathway.
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