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首页> 外文期刊>Cell Proliferation >Mineral trioxide aggregate upregulates odonto/osteogenic capacity of bone marrow stromal cells from craniofacial bones via JNK and ERK MAPK signalling pathways
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Mineral trioxide aggregate upregulates odonto/osteogenic capacity of bone marrow stromal cells from craniofacial bones via JNK and ERK MAPK signalling pathways

机译：三氧化二矿矿物质通过JNK和ERK MAPK信号通路上调颅面骨骨髓基质细胞的牙本质/成骨能力

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摘要

Objectives: The aim of this study was to investigate effects of mineral trioxide aggregate (MTA) on odonto/osteogenic differentiation of bone marrow stromal cells (BMSCs) from craniofacial bones. Materials and methods: Craniofacial BMSCs were isolated from rat mandible and effects of MTA on their proliferation, differentiation and MAPK pathway involvement were subsequently investigated, in vitro. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2,5-tetrazoliumbromide) assay was performed to evaluate proliferation of the MTA-treated cells. Alkaline phosphatase (ALP) activity, alizarin red staining, real-time reverse transcription polymerase chain reaction and western blot assays were used to assess differentiation capacity as well as MAPK pathway involvement. Results: 0.02 mg/ml MTA-treated BMSCs had significantly higher ALP activity and formed more mineralized nodules than the untreated group. Odonto/osteoblastic marker genes/proteins (Alp, Runx2/RUNX2, Osx/OSX, Ocn/OCN and Dspp/DSP respectively) in MTA-treated cells were remarkably upregulated compared to untreated ones. Mechanistically, phosphorylated Jun N-terminal kinase (P-JNK) and phosphorylated extracellular regulated protein kinases (P-ERK) in MTA-treated BMSCs increased significantly in a time-dependent manner, while inhibition of JNK and ERK MAPK pathways dramatically blocked MTA-induced odonto/osteoblastic differentiation, as indicated by reduced ALP levels, weakened mineralization capacity and downregulated levels of odonto/osteoblastic marker genes (Alp, Runx2, Osx, Ocn and Dspp). Conclusion: Mineral trioxide aggregate promoted odonto/osteogenic capacity of craniofacial BMSCs via JNK and ERK MAPK signalling pathways.
机译：目的：本研究的目的是研究三氧化二矿聚集体（MTA）对颅面骨骨髓基质细胞（BMSCs）的牙本质/成骨分化的影响。材料和方法：从大鼠下颌骨中分离出颅面BMSC，随后在体外研究MTA对它们的增殖，分化和MAPK途径参与的影响。进行MTT（3-（4,5-二甲基噻唑-2-基）-2,5-二苯基-2,5-四唑溴化物）测定以评估经MTA处理的细胞的增殖。碱性磷酸酶（ALP）活性，茜素红染色，实时逆转录聚合酶链反应和Western印迹法用于评估分化能力以及MAPK途径的参与。结果：0.02 mg / ml经MTA处理的BMSCs的ALP活性明显高于未处理组，并且形成了更多的矿化结节。与未经处理的细胞相比，经MTA处理的细胞中的Odonto /成骨细胞标记基因/蛋白质（分别为Alp，Runx2 / RUNX2，Osx / OSX，Ocn / OCN和Dspp / DSP）显着上调。从机理上讲，MTA处理的BMSC中磷酸化的Jun N末端激酶（P-JNK）和磷酸化的细胞外调节蛋白激酶（P-ERK）呈时间依赖性显着增加，而对JNK和ERK MAPK途径的抑制则显着阻断了MTA- ALP水平降低，矿化能力减弱和Odonto /成骨细胞标志物基因（Alp，Runx2，Osx，Ocn和Dspp）水平降低所表明的诱导牙本质/成骨细胞分化。结论：三氧化二矿聚集体通过JNK和ERK MAPK信号通路促进颅面BMSC的牙本质/成骨能力。

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