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Odontoblast β-catenin signaling regulates fenestration of mouse Hertwig's epithelial root sheath

查看全文 作　　者：ZHANG [1,2]Ran;TENG [2]Yan;ZHU [2]Liang;LIN [2]JingTing;YANG [2]Xiao;YANG [2]Guan;LI [1]TieJun 高影响力作者 机构地区：[1]Department of Oral Pathology, Peking University School and Hospital of Stomatology;[2]State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology高影响力机构 出　　处：《Science China(Life Sciences)》索引2015年第58卷第9期,共6页高影响力期刊 基　　金：supported by grants from the State Key Program of the National Natural Science Foundation of China(81030018);the National Basic Research Program of China(2012CB966904);the National Natural Science Foundation of China(30900863,81241062) 摘　　要：The interaction between Hertwig's epithelial root sheath(HERS) and the adjacent mesenchyme is vitally important in mouse tooth root development. We previously generated odontoblast-specific Ctnnb1(encoding β-catenin) deletion mice, and demonstrated that odontoblast β-catenin signaling regulates odontoblast proliferation and differentiation. However, the role of odontoblast β-catenin signaling in regulation of HERS behavior has not been fully investigated. Here, using the same odontoblast-specific Ctnnb1 deletion mice, we found that ablation of β-catenin signaling in odontoblasts led to aberrant HERS formation. Mechanistically, odontoblast-specific Ctnnb1 deletion resulted in elevated bone morphogenetic protein 7(Bmp7) expression and reduced expression of noggin and follistatin, both of which encode extracellular inhibitors of BMPs. Furthermore, the levels of phosphorylated Smad1/5/8 were increased in HERS cells. In vitro tissue culture confirmed that BMP7 treatment disrupted the HERS structure. Taken together, we demonstrated that odontoblast β-catenin signaling may act through regulation of BMP signaling to maintain the integrity of HERS cells. 关 键 词：成牙本质细胞 骨形态发生蛋白 信号调节 小鼠 Β-CATENIN 上皮 细胞特异性 开窗
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