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MEF2转录因子调控牙髓干细胞的成骨分化

MEF2 Transcription Factor Regulates Osteogenic Differentiation of Dental Pulp Stem Cells.

作者信息

Shen Shuling, Huang Dan, Feng Guijuan, Zhu Linhe, Zhang Ye, Cao Peipei, Zheng Ke, Zhang Dongmei, Feng Xingmei

机构信息

1 The Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University , Nantong, China .

2 Department of Stomatology, Affiliated Hospital of Nantong University , Nantong, China .

出版信息

Cell Reprogram. 2016 Aug;18(4):237-45. doi: 10.1089/cell.2016.0016.

DOI:10.1089/cell.2016.0016
PMID:27459583
Abstract

The myocyte enhancer factor-2 (MEF2) is a member of the MADS-box family. It controls the expression of genes that are critical for biological processes such as proliferation, cell death, and differentiation. Some studies have shown that MEF2 expression is enhanced in osteogenic progenitor cells established from bone marrow stromal cells with other types of mesenchymal progenitor cells. However, the effect of MEF2 on dental pulp stem cells (DPSCs) is unclear. In this study, we investigate the effect of MEF2 on regulating osteogenic differentiation and proliferation of DPSCs. We find that MEF2 is stably expressed in DPSCs, and the expression is increased time-dependently along with cell osteogenic differentiation. MEF2 expression also increases the alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2) activity, and enhances mineralization in DPSCs. SB202190, inhibitor of p38, blocks the p38/MEF2 pathway and osteogenic differentiation. In addition, MEF2 overexpression inhibits DPSC proliferation. In summary, our data indicate that MEF2 not only regulates DPSCs as an inhibitor of cell proliferation but is also a promoter of osteogenic differentiation through the p38/MEF2 signaling pathway.

摘要

肌细胞增强因子2(MEF2)是MADS盒家族的成员。它控制着对增殖、细胞死亡和分化等生物过程至关重要的基因的表达。一些研究表明,在从骨髓基质细胞与其他类型间充质祖细胞建立的成骨祖细胞中,MEF2表达增强。然而,MEF2对牙髓干细胞(DPSC)的影响尚不清楚。在本研究中,我们研究了MEF2对调节DPSC成骨分化和增殖的影响。我们发现MEF2在DPSC中稳定表达,并且随着细胞成骨分化,其表达呈时间依赖性增加。MEF2表达还增加了碱性磷酸酶(ALP)、 runt相关转录因子2(Runx2)的活性,并增强了DPSC中的矿化作用。p38抑制剂SB202190阻断p38/MEF2途径和成骨分化。此外,MEF2过表达抑制DPSC增殖。总之,我们的数据表明,MEF2不仅作为细胞增殖抑制剂调节DPSC,而且还是通过p38/MEF2信号通路促进成骨分化的因子。

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