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

作　　者：ZHANG Ran TENG Yan ZHU Liang LIN JingTing YANG Xiao YANG Guan LI TieJun 

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

出　　处：《Science China(Life Sciences)》2015年第9期876-881,共6页中国科学（生命科学英文版）

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 Ctnnbl （encodingβ-catenin） deletion mice, and demon- strated that odontoblast β-catenin signaling regulates odontoblast proliferation and differentiation. However, the role of odon- toblast β-catenin signaling in regulation of HERS behavior has not been fully investigated. Here, using the same odonto- blast-specific Ctnnbl deletion mice, we found that ablation of β-catenin signaling in odontoblasts led to aberrant HERS for- mation. Mechanistically, odontoblast-specific Ctnnbl deletion resulted in elevated bone morphogenetic protein 7 （Bmp7） ex- pression and reduced expression of noggin andfollistatin, both of which encode extracellular inhibitors of BMPs. Furthermore, the levels of phosphorylated Smadl/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 f3-catenin signaling may act through regula- tion of BMP signaling to maintain the integrity of HERS cells.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：Hertwig's epithelial root sheath β-catenin signaling BMP signaling mesenchyme-epithelium induction 

分 类 号：R781[医药卫生—口腔医学]