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首页> 外文期刊>Molecular Biology Reports >Mineral trioxide aggregate promotes odontoblastic differentiation via mitogen-activated protein kinase pathway in human dental pulp stem cells
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Mineral trioxide aggregate promotes odontoblastic differentiation via mitogen-activated protein kinase pathway in human dental pulp stem cells

机译:三氧化二矿物质聚集体通过人牙髓干细胞中的促分裂原激活的蛋白激酶途径促进牙本质细胞分化

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摘要

Mitogen-activated protein kinase (MAPK) pathways are involved in stem cell differentiation. However, the odontoblastic differentiation-inducing effects by mineral trioxide aggregate (MTA) via MAPK pathways have not been clarified in human dental pulp stem cells (DPSCs). In this study we investigated the effects of MTA on cell viability and production of differentiation markers, and the involvement of MAPK signaling pathways in cultured human DPSCs. Cells were cultured with MTA, and the viability and differentiation productions of the cells were determined using the MTT assay and real-time PCR analysis, respectively. MAPK activation was measured by western blotting. MTA at concentrations of 20 and 10 mg/ml was toxic for human DPSCs. MTA significantly increased the expression of alkaline phosphatase (ALP), dentin sialophosphoprotein (DSPP), type I collagen (COLI), osteocalcin (OCN) and bone sialoprotein (BSP) mRNAs and induced the phosphorylation of p42 and p44 (p42/44), p38 and c-Jun N-terminal kinases 1 and 2 (JNK1/2) MAPK. Furthermore, the inhibitor of p42/44 MAPK attenuated the MTA-induced odontoblastic differentiation. These data indicated that MTA-induced odontoblastic differentiation of human DPSCs was via MAPK pathways, which may play a key role in the repair responses of dentin-pulp-like complexes.
机译:丝裂原激活的蛋白激酶(MAPK)通路参与干细胞分化。然而,在人类牙髓干细胞(DPSCs)中,尚不清楚通过MAPK途径由三氧化二矿聚集体(MTA)诱导牙本质成骨分化的作用。在这项研究中,我们调查了MTA对细胞活力和分化标志物的产生以及MAPK信号通路在培养的人DPSC中的影响。用MTA培养细胞,并分别使用MTT测定法和实时PCR分析法测定细胞的活力和分化产生。通过蛋白质印迹测量MAPK激活。浓度为20和10 mg / ml的MTA对人DPSC有毒。 MTA显着增加了碱性磷酸酶(ALP),牙本质唾液磷蛋白(DSPP),I型胶原蛋白(COLI),骨钙蛋白(OCN)和骨唾液蛋白(BSP)mRNA的表达,并诱导了p42和p44的磷酸化(p42 / 44), p38和c-Jun N末端激酶1和2(JNK1 / 2)MAPK。此外,p42 / 44 MAPK抑制剂减弱了MTA诱导的齿质分化。这些数据表明,MTA诱导人DPSC的牙本质成骨分化是通过MAPK途径,这可能在牙本质浆样复合物的修复反应中起关键作用。

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