Abstract
BackgroundTissue regeneration mediated by mesenchymal stem cells (MSCs) is deemed a desirable way to repair teeth and craniomaxillofacial tissue defects. Nevertheless, the molecular mechanisms about cell proliferation and committed differentiation of MSCs remain obscure. Previous researches have proved that lysine demethylase 2A (KDM2A) performed significant function in the regulation of MSC proliferation and differentiation. SNRNP200, as a co-binding factor of KDM2A, its potential effect in regulating MSCs’ function is still unclear. Therefore, stem cells from the apical papilla (SCAPs) were used to investigate the function of SNRNP200 in this research.MethodsThe alkaline phosphatase (ALP) activity assay, Alizarin Red staining, and osteogenesis-related gene expressions were used to examine osteo−/dentinogenic differentiation potential. Carboxyfluorescein diacetate, succinimidyl ester (CFSE) and cell cycle analysis were applied to detect the cell proliferation. Western blot analysis was used to evaluate the expressions of cell cycle-related proteins.ResultsDepletion of SNRNP200 caused an obvious decrease of ALP activity, mineralization formation and the expressions of osteo−/dentinogenic genes including RUNX2, DSPP, DMP1 and BSP. Meanwhile, CFSE and cell cycle assays revealed that knock-down of SNRNP200 inhibited the cell proliferation and blocked cell cycle at the G2/M and S phase in SCAPs. In addition, it was found that depletion of SNRNP200 up-regulated p21 and p53, and down-regulated the CDK1, CyclinB, CyclinE and CDK2.ConclusionsDepletion of SNRNP200 repressed osteo−/dentinogenic differentiation potentials and restrained cell proliferation through blocking cell cycle progression at the G2/M and S phase, further revealing that SNRNP200 has crucial effects on preserving the proliferation and differentiation potentials of dental tissue-derived MSCs.
Highlights
Tissue regeneration mediated by mesenchymal stem cells (MSCs) is deemed a desirable way to repair teeth and craniomaxillofacial tissue defects
We adopted an assay to investigate whether SNRNP200 affects the function of Mesenchymal stem cells (MSCs) by using Stem cells from the apical papilla (SCAPs), and we found that depletion of SNRN P200 suppressed the osteo−/dentinogenic differentiation and the cell proliferation potentials of SCAPs
The results showed that 19 candidate ligand proteins were differentially expressed in SCAPs in hypoxia group compared to normoxic group (Supplementary Table 1)
Summary
Tissue regeneration mediated by mesenchymal stem cells (MSCs) is deemed a desirable way to repair teeth and craniomaxillofacial tissue defects. Mesenchymal stem cells (MSCs) possess the characteristics of immunoregulation, multi-directional differentiation potential, easy access, rapid proliferation in vitro, low activity loss after cryopreservation, low immunogenicity and non-toxic side effects. They have become the most commonly used seed cells for repairing damaged tissue in tissue engineering [1]. The formation of certain tissues and the production of a sufficient number of cells depend on the expression of specific genes and the activation of sequential signals. Understanding these signals is conducive to regeneration of desired tissues. It is essential to explore the molecular regulation mechanisms of MSCs
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