Figure 5: The models of miR-23a cluster in osteocyte differentiation. | Nature Communications

Figure 5: The models of miR-23a cluster in osteocyte differentiation.

From: MicroRNA miR-23a cluster promotes osteocyte differentiation by regulating TGF-β signalling in osteoblasts

Figure 5

(a) A schematic model of miR-23a cluster/Prdm16/TGF-β signalling axis. In the absence of miR-23a cluster, Prdm16 forms a negative complex with phosphorylated Smad2/3 and is recruited to the promoter of Smad-binding element (SBE) to suppress downstream target genes such as Sost. When miR-23a cluster is upregulated during osteoblast differentiation, Prdm16 is suppressed by the miR-23a cluster in a direct manner, which leads to increased H3 acetylation in the regulatory region, followed by induction of Sost by the phosphorylated Smad2/3 complex. (b) A model of regulation of osteocyte differentiation by the miR-23a cluster. During mature osteoblast to osteocyte differentiation, the miR-23a cluster suppresses Prdm16, a negative regulator of TGF-β signalling and enhances TGF-β signalling to accelerate osteocyte differentiation. The miR-23a cluster also downregulates other targets, such as Satb2, one of the osteoblast transcription factors. The role of the miR-23a cluster at the early stages of osteoblast differentiation is not clear yet. MSC, mesenchymal stem cell.

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