ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
Anti-inflammatory capacity of Apremilast in human chondrocytes is dependent on SOX-9.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Engineered Chondrocalcin From Pichia pastoris: A Dual-Functional Biomaterial for Cartilage Regeneration and Rheumatoid Arthritis Modulation.Biotechnology and bioengineering · 2026Article
- Repurposing apremilast for alzheimer's disease: multitarget modulation of cAMP‑PI3K/Akt-GSK‑3β and NF‑κB signaling.Metabolic brain disease · 2026Review
- Phosphodiesterase inhibitors as emerging therapeutics for skeletal disorders: A comprehensive review of mechanisms and repurposing potential.Bone reports · 2026Review
- Single-Cell Transcriptomics Reveals Riluzole as an Osteoarthritis Candidate Drug via OB-NE Signaling Modulation and CTSS/NOS1 Inhibition.Drug design, development and therapy · 2026Article
- Therapeutic potential of SOX family transcription factors in osteoarthritis.Annals of medicine · 2025Review
- Apremilast in osteoarthritis: exploring its therapeutic mechanisms.Drugs in context · 2025Review
- FABP4 knockdown suppresses inflammation, apoptosis and extracellular matrix degradation in IL-1β-induced chondrocytes by activating PPARγ to regulate the NF-κB signaling pathway.Molecular medicine reports · 2021Article
- Apremilast mitigates interleukin (IL)-13-induced inflammatory response and mucin production in human nasal epithelial cells (hNECs).Bioengineered · 2021Article
- Vorinostat ameliorates IL-1α-induced reduction of type II collagen by inhibiting the expression of ELF3 in chondrocytes.Journal of biochemical and molecular toxicology · 2021Article
- Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
background and purposeOsteoarthritis (OA) impacts the quality of life in middle-aged and elderly people by inducing immobility. The severe inflammation in chondrocytes is reported to be related to the development and process of OA. The present study aims to investigate the protective effects of Apremilast on injured chondrocytes induced by interleukin-1α (IL-1α) and the underlying mechanism.
methods10 ng/mL IL-1α was used to induce the in vitro injured chondrocytes. QRT-PCR was used to evaluate the expression level of Sry-type high-mobility-group box 9 (SOX-9), collagen type II alpha-1 gene (COL2A1), Aggrecan (ACAN) and collagen type X alpha 1 chain (COL10A1). SiRNA technology was utilized to knock down the expression of SOX-9 in the chondrocytes. The expression of SOX-9 was determined by Western Blot assay and/or immunofluorescence assay. Western Blot was used to evaluate the expression level of phosphorylated cyclic AMP response element binding (CREB).
resultsSOX9, Col2a1 and Acan were significantly up-regulated and Col10a1 was significantly down-regulated in the chondrocytes by Apremilast in a dose-dependent manner. IL-1α induced the injured chondrocytes by decreasing the expression of SOX9, Col2a1, Acan and increasing the expression of Col10a1, which were greatly reversed by Apremilast. By silencing SOX-9, the effects of Apremilast on SOX9 and marker genes were abolished. Phosphorylated CREB was up-regulated by Apremilast in a time-dependent manner. The up-regulated SOX-9 by Apremilast was reversed by the protein kinase A (PKA)/CREB pathway inhibitor H89.
conclusionApremilast may protect chondrocytes from inflammation by up-regulating SOX9.
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