Melatonin exhibits a variety of regulatory properties by binding to specific receptors and downstream molecules, and exerts a myriad of receptor-independent actions via intracellular targets as a chondrocyte protector, an anti-inflammation modulator, and a free radical scavenger. Although conventional pharmaceutical therapies aim to prevent further cartilage loss and joint dysfunction, there are no ideal strategies that target the pathogenesis of OA. Osteoarthritis (OA), the most common arthritis worldwide, is a degenerative joint disease characterized by progressive cartilage breakdown, subchondral remodeling, and synovial inflammation. SNRNP200, a co-binding protein of METTL7A, promoted the odontogenic differentiation of DPSCs. METTL7A promoted the odontogenic differentiation of DPSCs. The binding site of miR-6807-5p was the 3′UTR region of METTL7A, which was silenced by miR-6807-5p. The knockdown of SNRNP200 inhibited the odontogenic differentiation of DPSCs.Ĭonclusion: This study verified that miR-6807-5p inhibited the odontogenic differentiation of DPSCs. SNRNP200 was the co-binding protein of METTL7A. After mineralized induction, the odontogenic differentiation was weakened in the METTL7A-knockdown group and enhanced in the METTL7A-overexpressed group compared with the control group. METTL7A was the downstream target of miR-6807-5p. Results: After mineralized induction, the odontogenic differentiation was enhanced in the miR-6807-5p-knockdown group and weakened in the miR-6807-5p-overexpressed group compared with the control group.
Protein mass spectrometry and co-immunoprecipitation (Co-IP) were used to detect that SNRNP200 was the co-binding protein of METTL7A. Real-time RT-PCR, western blot, dual-luciferase reporter assay, and pull-down assay with biotinylated miRNA were used to confirm that METTL7A was the downstream gene of miR-6807-5p. Alkaline phosphatase (ALP), Alizarin red staining (ARS), and calcium ion quantification were used to detect the odontogenic differentiation of miR-6807-5p and METTL7A.
Methods: In this study, human dental pulp stem cells (DPSCs) were used. In this study, we intended to explore the function and mechanism of miR-6807-5p and its target gene METTL7A in odontogenic differentiation. Although the known regulatory mechanism and some achievements have been discovered, directional differentiation cannot effectively induce regeneration of tooth tissue.
Background: Tooth tissue regeneration mediated by mesenchymal stem cells (MSCs) has become the most ideal treatment.
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