ArticleMolecular medicine reports2016
Trichostatin A increases the TIMP-1/MMP ratio to protect against osteoarthritis in an animal model of the disease.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Ameliorative effect of Gastrodia elata Blume extract on inflammation in a rat model of osteoarthritis.Laboratory animal research · 2026Article
- Extracellular vesicles from human adipose-derived stem cells relieve pain and inflammation in a rat model of knee osteoarthritis.Stem cell research & therapy · 2026Article
- Rapid restoration of cell phenotype and matrix forming capacity following transient nuclear softening.Acta biomaterialia · 2025Article
- Epigenetic Biomarkers in Temporomandibular Joint Osteoarthritis: An Emerging Target in Treatment.International journal of molecular sciences · 2025Review
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- Landscape of Histone Posttranslational Modifications in Osteoarthritis.Journal of inflammation research · 2025Review
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- Krüppel-like factor-4 and Krüppel-like factor-2 are important regulators of joint tissue cells and protect against tissue destruction and inflammation in osteoarthritis.Annals of the rheumatic diseases · 2022Article
- Epigenetic Regulation of Chondrocytes and Subchondral Bone in Osteoarthritis.Life (Basel, Switzerland) · 2022Review
- Production of Mesenchymal Progenitor Cell-Derived Extracellular Vesicles in Suspension Bioreactors for Use in Articular Cartilage Repair.Stem cells translational medicine · 2022Article
- Histone deacetylase inhibitors attenuated interleukin-1β-induced chondrogenesis inhibition in synovium-derived mesenchymal stem cells of the temporomandibular joint.Bone & joint research · 2022Article
- The protective mechanism of SIRT1 on cartilage through regulation of LEF-1.BMC musculoskeletal disorders · 2021Article
- Activation of GPR40 Suppresses AGE-Induced Reduction of Type II Collagen and Aggrecan in Human SW1353 Chondrocytes.Drug design, development and therapy · 2020Article
- Article
- Sitagliptin ameliorates advanced glycation end-product (AGE)-induced degradation of extracellular matrix in human primary chondrocytes.American journal of translational research · 2019Article
- Inhibition of P2Y11R ameliorated TNF-α-induced degradation of extracellular matrix in human chondrocytic SW1353 cells.American journal of translational research · 2019Article
- The protective effects of exenatide against AGEs-induced articular matrix degradation in human primary chondrocytes.American journal of translational research · 2019Article
- The biomechanical and histological effects of posterior cruciate ligament rupture on the medial tibial plateau.Journal of orthopaedic surgery and research · 2017Article
- Protective Effects of Garlic-Derived S-Allylmercaptocysteine on IL-1BioMed research international · 2017Article
- REG3A promotes the proliferation, migration, and invasion of gastric cancer cells.OncoTargets and therapy · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone deacetylase inhibitor trichostatin A (TSA) has been demonstrated to alleviate certain symptoms associated with osteoarthritis (OA). However, the exact mechanisms underlying this protective effect remain to be elucidated. The present study therefore examined the effects of TSA on the expression levels of interleukin‑1β (IL‑1β)-induced matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in vitro and in vivo. In vitro, reverse transcription‑quantitative polymerase chain reaction was performed to investigate alterations in mRNA expression levels in TSA-treated chondrocytes in the presence or absence of IL‑1β; in addition, protein expression and acetylation levels were assessed by western blotting. In vivo, TSA was administered to rats by intra‑articular injection, following which the mRNA and protein expression levels were analyzed. In addition, macroscopic and histological observations were conducted. Chondrocytes treated with IL‑1β demonstrated increased mRNA and protein expression levels of MMP‑1, MMP‑3 and MMP-13, and decreased expression levels of TIMP‑1 mRNA and protein; these alterations were significantly attenuated by TSA treatment. In addition, increased MMPs and decreased TIMP‑1 expression levels were observed in vivo in the OA rat model. TSA treatment demonstrated in vivo efficacy through the attenuation of various OA‑associated molecular and physiological changes. Taken together, the results of the present study suggest that TSA has potential therapeutic value for the treatment of OA.
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