ArticleActa biochimica et biophysica Sinica2023
HDAC6 inhibition regulates substrate stiffness-mediated inflammation signaling in chondrocytes.
Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Pulsatile low shear stress increases susceptibility to endothelial inflammation via upregulation of IFT and activation of YAP.APL bioengineering · 2025Article
- Primary cilia and inflammatory response: unveiling new mechanisms in osteoarthritis progression.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- [Piezo1 Mediates the Regulation of Substrate Stiffness on Primary Cilia in Chondrocytes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- Novel mechanistic study of HDAC6 regulation of rheumatoid arthritis via CMA: exploring potential therapeutic targets.Frontiers in pharmacology · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a chronic disease and is difficult to cure. Chondrocytes are highly mechanosensitive. Therefore, mechanical therapies have received attention as a therapeutic direction for OA. The stiffness, as a critical cue of the extracellular matrix (ECM), affects cell growth, development, and death. In this study, we use polydimethylsiloxane (PDMS) to create substrates with varying stiffness for chondrocyte growth, interleukin-1β (IL-1β) treatment to mimic the inflammatory environment, and Tubastatin A (Tub A) to inhibit histone deacetylase 6 (HDAC6). Our results show that stiff substrates can be anti-inflammatory and provide a better matrix environment than soft substrates. Inhibition of HDAC6 improves the inflammatory environment caused by IL-1β and coordinates with inflammation to spread the chondrocyte area and primary cilia elongation. Without IL-1β and Tub A treatments, the length of the primary cilia rather than frequency is stiffness-dependent, and their length on stiff substrates are greater than that on soft substrates. In conclusion, we demonstrate that stiff substrates, inflammation, and inhibition of HDAC6 enhance the mechanosensitivity of primary cilia and mediate substrate stiffness to suppress inflammation and protect the matrix.
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