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10.1016/j.jare.2025.09.002 http://scihub22266oqcxt.onion/10.1016/j.jare.2025.09.002 40914424!ä!40914424 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=40914424&cmd=llinks): Failed to open stream: HTTP request failed! 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HDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis in temporomandibular joint osteoarthritis |pdf=|usr=}}{{40914424}} gab.com Text HDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis in temporomandibular joint osteoarthritis JO: J Adv Res http://www.kidney.de/pget.php?&tw=1&pmid=40914424 #FOAvip INTRODUCTION: Aberrant biomechanical force-induced chondrocyte adipogenesis is involved in the development of temporomandibular joint osteoarthritis (TMJ OA). Growth differentiation factor 11 (GDF11) has been implicated in this process. However, whether mechanosensitive histone deacetylase 3 (HDAC3) regulates GDF11 signaling in the context of TMJ OA remains to be elucidated. OBJECTIVE: To elucidate the HDAC3-mediated regulation of GDF11 during chondrocyte adipogenesis in TMJ OA. METHODS: A unilateral anterior crossbite (UAC) rat model and cyclic tensile strain (CTS)-stimulated ATDC5 cells were established to mimic aberrant biomechanical force. Cartilage degeneration was assessed via Safranin O staining and qRT-PCR. Chondrocyte adipogenesis was evaluated using Oil Red O staining, transmission electron microscopy (TEM), and Adiponectin immunohistochemistry (IHC). The expression of HDAC3, nuclear factor erythroid 2-related factor 2 (Nrf2), and GDF11 was quantified by IHC, qRT-PCR, and western blotting. The binding of Nrf2 to GDF11 was evaluated by dual-luciferase reporter assays. The therapeutic interventions included intra-articular injections of the HDAC3 inhibitor RGFP966 (10?mg/kg) and the Nrf2 agonist Bardoxolone (10?mg/kg). RESULTS: The articular cartilage was significantly thinner, the modified Osteoarthritis Research Society International (OARSI) scores were increased, the expression of cartilage matrix markers (collagen II and Aggrecan) was reduced, and the expression of chondrocyte hypertrophic markers (collagen?X,?matrix metalloprotease-13, and alkaline phosphatase) was increased in the UAC-induced OA model group compared with the sham control group. Excessive biomechanical force accelerated chondrocyte adipogenesis, as indicated by increased lipid droplet accumulation and Adiponectin upregulation. Concurrently, HDAC3 was upregulated, which suppressed Nrf2 and downregulated GDF11. Dual-luciferase reporter assays confirmed the direct binding of Nrf2 to the GDF11 promoter in chondrocytes. Treatment with the HDAC3 inhibitor RGFP966 or the Nrf2 agonist Bardoxolone restored GDF11 expression, significantly attenuating adipogenesis and alleviating cartilage degeneration. CONCLUSIONS: Our findings indicate that aberrant biomechanical force induces HDAC3 upregulation, which suppresses Nrf2-mediated transactivation of GDF11, thereby promoting chondrocyte adipogenesis and exacerbating TMJ OA progression. Twit Text FOAVip HDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis in temporomandibular joint osteoarthritis ????J Adv Res http://www.kidney.de/pget.php?&tw=1&pmid=40914424 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=40914424 #FOAvip English Wikipedia <ref>{{Cite pmid|40914424}}</ref> HDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis in temporomandibular joint osteoarthritis #MMPMID40914424 Shi Y; Xu Z; Li F; Liu Q; Zhan Y; Wu F; Li Q; He F; Fan P; Zhang H; Yu S; He F; Wang H; Zhang M J Adv Res 2025[Sep]; ä (ä): ä PMID40914424show ga INTRODUCTION: Aberrant biomechanical force-induced chondrocyte adipogenesis is involved in the development of temporomandibular joint osteoarthritis (TMJ OA). Growth differentiation factor 11 (GDF11) has been implicated in this process. However, whether mechanosensitive histone deacetylase 3 (HDAC3) regulates GDF11 signaling in the context of TMJ OA remains to be elucidated. OBJECTIVE: To elucidate the HDAC3-mediated regulation of GDF11 during chondrocyte adipogenesis in TMJ OA. METHODS: A unilateral anterior crossbite (UAC) rat model and cyclic tensile strain (CTS)-stimulated ATDC5 cells were established to mimic aberrant biomechanical force. Cartilage degeneration was assessed via Safranin O staining and qRT-PCR. Chondrocyte adipogenesis was evaluated using Oil Red O staining, transmission electron microscopy (TEM), and Adiponectin immunohistochemistry (IHC). The expression of HDAC3, nuclear factor erythroid 2-related factor 2 (Nrf2), and GDF11 was quantified by IHC, qRT-PCR, and western blotting. The binding of Nrf2 to GDF11 was evaluated by dual-luciferase reporter assays. The therapeutic interventions included intra-articular injections of the HDAC3 inhibitor RGFP966 (10?mg/kg) and the Nrf2 agonist Bardoxolone (10?mg/kg). RESULTS: The articular cartilage was significantly thinner, the modified Osteoarthritis Research Society International (OARSI) scores were increased, the expression of cartilage matrix markers (collagen II and Aggrecan) was reduced, and the expression of chondrocyte hypertrophic markers (collagen?X,?matrix metalloprotease-13, and alkaline phosphatase) was increased in the UAC-induced OA model group compared with the sham control group. Excessive biomechanical force accelerated chondrocyte adipogenesis, as indicated by increased lipid droplet accumulation and Adiponectin upregulation. Concurrently, HDAC3 was upregulated, which suppressed Nrf2 and downregulated GDF11. Dual-luciferase reporter assays confirmed the direct binding of Nrf2 to the GDF11 promoter in chondrocytes. Treatment with the HDAC3 inhibitor RGFP966 or the Nrf2 agonist Bardoxolone restored GDF11 expression, significantly attenuating adipogenesis and alleviating cartilage degeneration. CONCLUSIONS: Our findings indicate that aberrant biomechanical force induces HDAC3 upregulation, which suppresses Nrf2-mediated transactivation of GDF11, thereby promoting chondrocyte adipogenesis and exacerbating TMJ OA progression. äHDAC3 represses Nrf2-GDF11 signaling to drive chondrocyte adipogenesis(epmc).pdf DeepDyve Pubget Overpricing