ArticleInflammation2020
Suberoylanilide Hydroxamic Acid Attenuates Interleukin-1β-Induced Interleukin-6 Upregulation by Inhibiting the Microtubule Affinity-Regulating Kinase 4/Nuclear Factor-κB Pathway in Synovium-Derived Mesenchymal Stem Cells from the Temporomandibular Joint.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Epigenetic Biomarkers in Temporomandibular Joint Osteoarthritis: An Emerging Target in Treatment.International journal of molecular sciences · 2025Review
- Review
- Inhibition of MARK4 Promotes Mitochondrial Biogenesis by Inducing the Phosphorylation of AMPKα to Reduce Myocardial Damage in Rats With Myocardial Infarction.Cardiology research and practice · 2025Article
- Role of MARK4 in methamphetamine-induced acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Navigating the Maze of Kinases: CaMK-like Family Protein Kinases and Their Role in Atherosclerosis.International journal of molecular sciences · 2024Review
- Qingzhuan dark tea Theabrownin alleviates hippocampal injury in HFD-induced obese mice through the MARK4/NLRP3 pathway.Heliyon · 2024Article
- Pan-histone deacetylase inhibitor vorinostat suppresses osteoclastic bone resorption through modulation of RANKL-evoked signaling and ameliorates ovariectomy-induced bone loss.Cell communication and signaling : CCS · 2024Article
- Article
- The Dual Role of Small Extracellular Vesicles in Joint Osteoarthritis: Their Global and Non-Coding Regulatory RNA Molecule-Based Pathogenic and Therapeutic Effects.Biomolecules · 2023Review
- Global Trends and Future Research Directions for Temporomandibular Disorders and Stem Cells.Journal of functional biomaterials · 2023Review
- Effects of interleukin 1β on long noncoding RNA and mRNA expression profiles of human synovial fluid derived mesenchymal stem cells.Scientific reports · 2022Article
- Potential mechanisms and therapeutic targets of mesenchymal stem cell transplantation for ischemic stroke.Stem cell research & therapy · 2022Review
- Evaluation of CD49f as a novel surface marker to identify functional adipose-derived mesenchymal stem cell subset.Cell proliferation · 2021Article
- An Update on Mesenchymal Stem Cell-Centered Therapies in Temporomandibular Joint Osteoarthritis.Stem cells international · 2021Review
- NLRP3 Blockade Suppresses Pro-Inflammatory and Pro-Angiogenic Cytokine Secretion in Diabetic Retinopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Synovium-derived mesenchymal stem cells (SMSCs) can migrate to the site of destroyed condylar cartilage and differentiate into chondrocytes to repair temporomandibular joint (TMJ) damage. Interleukin (IL)-1β-induced IL-6 secretion has been shown to inhibit the chondrogenic potential of SMSCs. The histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) has recently been shown to be closely related to the inflammation induced by IL-1β. However, the relationship between SAHA and IL-6 secretion induced by IL-1β in SMSCs remains unclear. In this study, we evaluated the relationships between IL-1β and IL-6 in synovial specimens from patients with TMD and in model rats with osteoarthritis (OA). We found that IL-1β and IL-6 were positively correlated and that IL-6 expression in SMSCs increased with IL-1β stimulation in vitro. Moreover, microtubule affinity-regulating kinase 4 (MARK4) was significantly upregulated in IL-1β-stimulated SMSCs and in the synovium of rats with OA. MARK4 knockdown inhibited IL-6 secretion and nuclear factor (NF)-κB pathway activation in IL-1β-stimulated SMSCs. SAHA attenuated IL-6 secretion in IL-1β-induced SMSCs through NF-κB pathway inhibition, and MARK4 was also downregulated in SAHA-treated SMSCs. However, inhibition of the NF-κB pathway did not suppress MARK4 expression. Thus, these results showed that SAHA attenuated IL-6 secretion in IL-1β-induced SMSCs through inhibition of the MARK4/NF-κB pathway.
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