ArticleJournal of cellular and molecular medicine2024
The N-terminal fragment of histone deacetylase 4 (1-669aa) promotes chondrocyte apoptosis via the p53-dependent endoplasmic reticulum stress pathway.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- The N-terminal fragment of histone deacetylase 4 (1-669aa) promotes chondrocyte apoptosis via the p53-dependent endoplasmic reticulum stress pathway.Journal of cellular and molecular medicine · 2024Article
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10 authors.
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Abstract
Exogenous administration of the histone deacetylation 4 (HDAC4) protein can effectively delay osteoarthritis (OA) progression. However, HDAC4 is unstable and easily degrades into N-terminal (HDAC4-NT) and C-terminal fragments, and the HDAC4-NT can exert biological effects, but little is known about its role in chondrocytes and cartilage. Thus, the roles of HDAC4-NT fragments (1-289aa, 1-326aa and 1-669aa) in chondrocytes and cartilage were evaluated via real-time cell analysis (RTCA), safranin O staining, Sirius Red staining and nanoindentation. Molecular mechanisms were profiled via whole-transcriptome sequencing (RNA-seq) and verified in vitro and in vivo by a live cell real-time monitoring system, flow cytometry, western blotting and immunohistochemistry. The results showed that 1-669aa induced chondrocyte death and cartilage injury significantly, and the differentially expressed genes (DEGs) were enriched mainly in the apoptotic term and p53 signalling pathway. The validation experiments showed that 1-669aa induced chondrocyte apoptosis via the endoplasmic reticulum stress (ERS) pathway, and up-regulated p53 expression was essential for this process. Thus, we concluded that the HDAC4-NT fragment 1-669aa induces chondrocyte apoptosis via the p53-dependent ERS pathway, suggesting that in addition to overexpressing HDAC4, preventing it from degradation may be a new strategy for the treatment of OA.
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