ArticleThe American journal of pathology2016
Histone Deacetylase Inhibitor Vorinostat (SAHA) Suppresses IL-1β-Induced Matrix Metallopeptidase-13 Expression by Inhibiting IL-6 in Osteoarthritis Chondrocyte.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Epigenetic research methods and animal models for intervertebral disc degeneration (Review).Molecular medicine reports · 2026Review
- Curcumin inhibits chondrocyte apoptosis and inflammation in osteoarthritis via the miR-338-3p/EIF4A1 signaling axis.Hereditas · 2026Article
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Mechanism of action of total saponin Achyranthes in treating knee osteoarthritis explored using network pharmacology and animal experimentation.Iranian journal of basic medical sciences · 2025Article
- Catalpol protects mouse ATDC5 chondrocytes against interleukin-1β-induced catabolism.Histology and histopathology · 2024Article
- Current understanding of osteoarthritis pathogenesis and relevant new approaches.Bone research · 2022Review
- Epigenetic therapy targeting bone marrow mesenchymal stem cells for age-related bone diseases.Stem cell research & therapy · 2022Review
- Restoration of the Phenotype of Dedifferentiated Rabbit Chondrocytes by Sesquiterpene Farnesol.Pharmaceutics · 2022Article
- Histone deacetylase inhibitors attenuated interleukin-1β-induced chondrogenesis inhibition in synovium-derived mesenchymal stem cells of the temporomandibular joint.Bone & joint research · 2022Article
- A retrotransposon gag-like-3 gene RTL3 and SOX-9 co-regulate the expression of COL2A1 in chondrocytes.Connective tissue research · 2021Article
- 4-Methylumbelliferone suppresses catabolic activation in anterior cruciate ligament-derived cells via a mechanism independent of hyaluronan inhibition.Journal of orthopaedic surgery and research · 2021Article
- The protective mechanism of SIRT1 on cartilage through regulation of LEF-1.BMC musculoskeletal disorders · 2021Article
- Histone Modifications and Chondrocyte Fate: Regulation and Therapeutic Implications.Frontiers in cell and developmental biology · 2021Review
- Article
- Epigenetic Therapies for Osteoarthritis.Trends in pharmacological sciences · 2020Review
- Expression profile of matrix metalloproteinases in the labrum of femoroacetabular impingement.Bone & joint research · 2020Article
- The Role of HDACs and HDACi in Cartilage and Osteoarthritis.Frontiers in cell and developmental biology · 2020Review
- HDAC10 upregulation contributes to interleukin 1β-mediated inflammatory activation of synovium-derived mesenchymal stem cells in temporomandibular joint.Journal of cellular physiology · 2019Article
- Epigenetics in osteoarthritis: Novel spotlight.Journal of cellular physiology · 2019Review
- Regulation of Chemokines and Cytokines by Histone Deacetylases and an Update on Histone Decetylase Inhibitors in Human Diseases.International journal of molecular sciences · 2019Review
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Abstract
Osteoarthritis (OA) is the most common whole-joint disease and is characterized by progressive loss of the cartilage matrix. Matrix metallopeptidase-13 (MMP-13) is a highly active and an abundantly expressed protease in OA cartilage and chondrocytes and degrades type II collagen and proteoglycans. We investigated the mechanism of MMP-13 suppression by histone deacetylase inhibitor vorinostat (SAHA). OA chondrocytes were obtained from knee cartilage after enzymatic digestion and treated with IL-1β in the absence or presence of various histone deacetylase inhibitors. Gene expression was quantified using quantitative RT-PCR. Protein expression and chromatin modifications were determined by Western immunoblotting using specific antibodies. The effect of IL-6 on the expression of MMP-13 was determined by treating chondrocytes with recombinant IL-6 or by IL6 knockdown using IL6-specific siRNA. We found that SAHA is a potent suppressor of IL-1β-induced MMP-13, tumor necrosis factor-α, and other catabolic marker expression in OA chondrocytes. Interestingly, SAHA rescued the COL2A1 and ACAN expression in OA chondrocytes that was down-regulated by IL-1β. Of importance is our finding that IL-6-stimulated MMP-13 expression was independent of IL-1β stimulation and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in OA chondrocytes. Taken together, our results suggest that SAHA could be used as a therapeutic agent for the management of OA.
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