Hdac4 Enhances Synovium-derived Stem Cell-based Chondrogenesis Induced by Tgf-β1

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Introduction Transforming growth factor beta (TGF-β) superfamily members play diverse roles in cartilage development and maintenance. TGF-β not only up-regulates a number of molecules associated with prechondrogenic condensation, it also up-regulates chondrogenic gene expression through several signaling pathways. Moreover, TGF-β has been reported to inhibit osteoblast differentiation by repressing runt-related transcription factor 2 (Runx 2) . However, our previous study indicated that TGF-β1 alone is not sufficient to fully differentiate mesenchymal stem cells (MSCs) into chondrocytes . Other factors are necessary for the chondrogenic differentiation process. Histone deacetylases (HDACs) are the enzymes catalyzing the deacetylation of histone and non-histone proteins and regulating cell proliferation, differentiation, and apoptosis. Recently, it was reported that HDAC4 acts as a negative regulator of chondrocyte hypertrophy . We hypothesize that HDAC4 may promote TGF-β1-induced stem cell-based chondrogenesis.

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تاریخ انتشار 2009