Role of Special AT-Rich Sequence-Binding Protein 2 in the Osteogenesis of Dental Mesenchymal Stem Cells
Role of Special AT-Rich Sequence-Binding Protein 2 in the Osteogenesis of Dental Mesenchymal Stem Cells
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富含AT的特殊序列结合蛋白2在牙间充质干细胞成骨中的作用
DOI：
10.1089/scd.2020.0013
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发表时间：
2020-06-25
影响因子：
4
通讯作者：
Zhang, Hongmei
中科院分区：
文献类型：
--
作者：
Chen, Qianyu;Lin, Juhong;Zhang, Hongmei
牙源性间充质干细胞（mesenchymal stem cells，MSCs）具有多向分化潜能、再生能力强、易于非侵入性获取等优点，被认为是修复颅面骨缺损的关键因素。SATB 2是一种核基质蛋白，参与染色质重塑和转录调控，并已被报道为成骨细胞分化、骨形成和骨髓间充质干细胞骨再生的正调控因子。在这项研究中，我们系统地研究了SATB 2促进牙周膜干细胞（PDLSC），牙髓干细胞（DPSC）和人脱落乳牙干细胞（SHED）的成骨分化的能力。RNA-seq分析和实时定量PCR（RT-PCR）显示，调控成骨分化的基因在三种细胞类型中差异表达，并发现SATB 2以相对较高的水平表达。当三种细胞类型过表达SATB 2与AdSATB 2感染，碱性磷酸酶（ALP）染色，ALP活性，茜素红S染色，和定量趋于增加感染率。而AdsiSATB 2感染后则表现出相反的结果。RT-PCR结果显示，SATB 2过表达后，Spp 1、Sema 7a、Atf 4、Ibsp、Col 1a 1、Sp 7、Igfbp 3、Dlx 3和Alpl等9个成骨基因表达量均不同程度上调。此外，定量PCR结果表明，SATB 2影响MSC标志物的表达。这些结果表明SATB 2在PDLSC、DPSC和SHED的成骨中起重要作用。进一步的研究是必要的，以调查SATB 2介导的成骨分化的调节，并评估SATB 2的有缺陷的颅面骨组织再生的治疗用途。
Dental mesenchymal stem cells (MSCs) are recognized as a critical factor in repair of defective craniofacial bone owing to the multiple differentiation potential, the ability to regenerate distinct tissues, and the advantage that they can be easily obtained by relatively noninvasive procedures. Special AT-rich sequence-binding protein 2 (SATB2) is a nuclear matrix protein, involved in chromatin remodeling and transcriptional regulation, and has been reported to be as a positive regulator of osteoblast differentiation, bone formation, and bone regeneration in MSCs. In this study, we systematically investigated the capability of SATB2 to promote the osteogenic differentiation of periodontal ligament stem cells (PDLSCs), dental pulp stem cells (DPSCs), and stem cells from human exfoliated deciduous teeth (SHED). RNA-seq analysis and quantitative real-time PCR (RT-PCR) revealed that genes regulating osteogenic differentiation were differentially expressed among three cell types and SATB2 was found to be expressed at a relatively high level. When the three cell types overexpressed SATB2 with AdSATB2 infection, alkaline phosphatase (ALP) staining, ALP activity, Alizarin Red S staining, and quantification tended to increase with an increasing infection rate. It showed opposite results after infection with AdsiSATB2. RNA-seq analysis indicated that the expression of downstream osteogenic genes was affected by AdSATB2 infection and quantitative RT-PCR confirmed that nine osteogenic genes (Spp1,Sema7a,Atf4,Ibsp,Col1a1,Sp7,Igfbp3,Dlx3, andAlpl) were upregulated, to various extents, following SATB2 overexpression. In addition, quantitative PCR results indicated that SATB2 affected the expression of MSC markers. These results suggested an important role of SATB2 in the osteogenesis of PDLSCs, DPSCs, and SHED. Further research is warranted to investigate SATB2-mediated regulation of osteogenic differentiation and to evaluate the therapeutic use of SATB2 for the regeneration of defective craniofacial bone tissue.