ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2015
Sam68 Promotes NF-κB Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Dissect Gender-Dependent Susceptibility SNPs in Progressive Osteoarthritis Using Regulator Motif Candidate of Genetic Association Strategy (RMCGA).International journal of molecular sciences · 2025Article
- Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024Review
- siRNA therapy in osteoarthritis: targeting cellular pathways for advanced treatment approaches.Frontiers in immunology · 2024Review
- Bioinformatics Analysis of Biomarkers and Therapeutic Targets Related to Necroptosis in Intervertebral Disc Degeneration.BioMed research international · 2024Article
- Sam68 promotes osteogenic differentiation of aortic valvular interstitial cells by TNF-α/STAT3/autophagy axis.Journal of cell communication and signaling · 2023Article
- Article
- Anti-inflammatory effects of mesenchymal stem cell-conditioned media inhibited macrophages activation in vitro.Scientific reports · 2022Article
- Relationship of mRNA Expression of Selected Genes in Peripheral Blood and Synovial Fluid in Cranial Cruciate Ligament Deficient Stifles of Dogs.Animals : an open access journal from MDPI · 2022Article
- Elucidation of Potential Targets of San-Miao-San in the Treatment of Osteoarthritis Based on Network Pharmacology and Molecular Docking Analysis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Probiotic Composition and Chondroitin Sulfate Regulate TLR-2/4-Mediated NF-κB Inflammatory Pathway and Cartilage Metabolism in Experimental Osteoarthritis.Probiotics and antimicrobial proteins · 2021Article
- Recent Developments in Clinical Applications of Mesenchymal Stem Cells in the Treatment of Rheumatoid Arthritis and Osteoarthritis.Frontiers in immunology · 2021Review
- Clusterin exerts a cytoprotective and antioxidant effect in human osteoarthritic cartilage.Aging · 2020Article
- The Role of Inflammation in the Pathogenesis of Osteoarthritis.Mediators of inflammation · 2020Review
- STAT3 speeds up progression of osteoarthritis through NF-κB signaling pathway.Experimental and therapeutic medicine · 2020Article
- Review
- Protective Effect of Genistein on Condylar Cartilage through Downregulating NF-BioMed research international · 2019Article
- Role of Forkhead Box O Transcription Factors in Oxidative Stress-Induced Chondrocyte Dysfunction: Possible Therapeutic Target for Osteoarthritis?International journal of molecular sciences · 2018Review
- Hesperidin protects against IL-1β-induced inflammation in human osteoarthritis chondrocytes.Experimental and therapeutic medicine · 2018Article
- Exploring the Key Genes and Pathways of Osteoarthritis in Knee Cartilage in a Rat Model Using Gene Expression Profiling.Yonsei medical journal · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-κB activation and apoptosis signaling in OA articular chondrocytes.
methodsSam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-α) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-α stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-κB activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-α-treated chondrocytes for p65 and Sam68.
resultsSam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-α stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-α-stimulation. Sam68 knockdown suppressed Iκ-B degradation and p65 nuclear transportation in TNF-α-treated chondrocytes, indicating a suppressed NF-κB activation. Upon TNF-α exposure, the nuclear transportation of Sam68 and its interaction with p65 was detected in chondrocytes. Furthermore, Sam68 knockdown also alleviated the TNF-α-induced catabolic marker (MMP13, ADAMTS5, iNOS and IL-6) expression.
conclusionsThe highly expressed Sam68 promotes NF-κB signaling activation, catabolic gene expression and cellular apoptosis in TNF-α-treated chondrocytes, which may provide better insights into the pathophysiology of OA and a potential target for its treatment.
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