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首页> 外文期刊>Life sciences >Mechanical stress promotes odontoblastic differentiation via the heme oxygenase-1 pathway in human dental pulp cell line.
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Mechanical stress promotes odontoblastic differentiation via the heme oxygenase-1 pathway in human dental pulp cell line.

机译：机械应力通过人牙髓细胞系中的血红素加氧酶-1途径促进牙本质细胞分化。

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摘要

AIMS: Although heme oxygenase-1 (HO-1) is involved in osteoblastic differentiation, the HO-1- and odontoblastic differentiation-inducing effects of mechanical stress (MS) have not been clarified in human dental pulp cells (HDPCs). In this study, we examined the effects of MS on the odontoblastic differentiation of immortalized HDPCs and on the primary intracellular signaling pathways, including the HO-1 pathway, implicated in this differentiation. MAIN METHODS: A Flexercell strain unit was used to generate cyclic tensile strain in HDPCs. Expressions of mRNAs encoding HO-1 and HDPC differentiation markers, such as osteopontin (OPN), bone sialoprotein (BSP), dentin sialophosphoprotein (DSPP), and dentin matrix-protein-1 (DMP-1), were evaluated using the reverse transcription-polymerase chain reaction. Expression of the NF-E2-related transcription factor 2 (Nrf2) protein was analyzed by Western blotting. KEY FINDINGS: MS significantly increased the expression of HO-1, OPN, BSP, DSPP, and DMP-1 mRNAs in HDPCs. HO-1 silencing and inhibitors of HO-1, p38 MAPK, ERK, phosphoinositide 3-kinase, and nuclear factor-kappaB (NF-kappaB) all attenuated MS-stimulated differentiation. The MS-induced nuclear translocation of Nrf2 was suppressed by inhibitors of PI3K and NF-kappaB. SIGNIFICANCE: Collectively, these results provide the first evidence that MS stimulates odontoblastic differentiation of HDPCs via modulation of the Nrf2-mediated HO-1 pathway.
机译：目的：尽管血红素加氧酶-1（HO-1）参与成骨细胞的分化，但在人类牙髓细胞（HDPC）中尚不清楚机械应力（MS）诱导HO-1和成牙本质细胞分化的作用。在这项研究中，我们检查了MS对永生化HDPC的齿质分化和对主要细胞内信号传导途径（包括HO-1途径）的影响。主要方法：Flexercell应变单元用于在HDPC中产生循环拉伸应变。使用逆转录方法评估了编码HO-1和HDPC分化标记的mRNA的表达，例如骨桥蛋白（OPN），骨唾液蛋白（BSP），牙本质唾液磷蛋白（DSPP）和牙本质基质蛋白-1（DMP-1）。 -聚合酶链反应。通过蛋白质印迹分析了NF-E2相关转录因子2（Nrf2）蛋白的表达。主要发现：MS可显着增加HDPC中HO-1，OPN，BSP，DSPP和DMP-1 mRNA的表达。 HO-1沉默和HO-1抑制剂，p38 MAPK，ERK，磷酸肌醇3激酶和核因子-κB（NF-κB）均减弱了MS刺激的分化。 MS诱导的Nrf2核易位受到PI3K和NF-κB抑制剂的抑制。意义：总的来说，这些结果提供了第一个证据，表明MS通过调节Nrf2介导的HO-1途径刺激了HDPC的齿质分化。

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