牙上皮间充质Wnt/β-catenin信号传导诱导Wnt和BMP拮抗剂。

IF 1.6 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Organogenesis Pub Date : 2019-01-01 Epub Date: 2019-06-26 DOI:10.1080/15476278.2019.1633871
Xiaoyan Chen, Jing Liu, Nan Li, Yu Wang, Nan Zhou, Lei Zhu, Yiding Shi, Yingzhang Wu, Jing Xiao, Chao Liu
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引用次数: 7

摘要

先前的研究表明,间质Wnt/β-catenin信号的升高剥夺了牙间质成牙的命运。通过离体或药理学方法,发现发育中的牙间质中Wnt/β-catenin信号通过破坏Axin2和Runx2之间的平衡来抑制牙源性命运。在我们的研究中,Osr2-creKI;以Ctnnb1ex3f小鼠为研究对象,探讨体内间充质Wnt/β-catenin信号通路如何抑制成牙命运。我们发现osr2的所有门牙和一半的磨牙细菌;ctnnb1ex3f小鼠在E14.5开始退化,在出生时几乎消失。Fgf3和Msx1在E14.5 Osr2-creKI中的表达显著下调;而runx2转录仅在门牙间质中减少。有趣的是,在E14.5 Osr2-creKI;ctnnb1ex3切牙上皮中,Noggin的表达被激活,而Shh的表达被取消。同样,Wnt和BMP拮抗剂Ectodin和Noggin在E14.5 Osr2-creKI中也被异位激活;Ctnnb1ex3f磨牙上皮。E13.5 Osr2-creKI基因的重组Ctnnb1ex3f磨牙间充质与E10.5和E13.5 WT牙上皮不能发育成牙。综上所述,间充质Wnt/β-catenin信号传导不仅直接抑制成牙基因的表达,还在牙上皮中诱导Wnt和BMP拮抗剂,从而导致体内成牙命运的丧失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium.

Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium.

Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium.

Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium.

Previous studies indicated that the elevated mesenchymal Wnt/β-catenin signaling deprived dental mesenchyme of odontogenic fate. By utilizing ex vivo or pharmacological approaches, Wnt/β-catenin signaling in the developing dental mesenchyme was suggested to suppress the odontogenic fate by disrupting the balance between Axin2 and Runx2. In our study, the Osr2-creKI; Ctnnb1ex3f mouse was used to explore how mesenchymal Wnt/β-catenin signaling suppressed the odontogenic fate in vivo. We found that all of the incisor and half of the molar germs of Osr2-creKI; Ctnnb1ex3fmice started to regress at E14.5 and almost disappeared at birth. The expression of Fgf3 and Msx1 was dramatically down-regulated in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor and molar mesenchyme, while Runx2transcription was only diminished in incisor mesenchyme. Intriguingly, in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor epithelium, the expression of Noggin was activated, while Shh was abrogated. Similarly, the Wnt and BMP antagonists, Ectodin and Noggin were also ectopically activated in the E14.5 Osr2-creKI; Ctnnb1ex3f molar epithelium. Recombination of E13.5 Osr2-creKI; Ctnnb1ex3f molar mesenchyme with E10.5 and E13.5 WT dental epithelia failed to develop tooth. Taken together, the mesenchymal Wnt/β-catenin signaling resulted in the loss of odontogenic fate in vivo not only by directly suppressing odontogenic genes expression but also by inducing Wnt and BMP antagonists in dental epithelium.

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来源期刊
Organogenesis
Organogenesis BIOCHEMISTRY & MOLECULAR BIOLOGY-DEVELOPMENTAL BIOLOGY
CiteScore
4.10
自引率
4.30%
发文量
6
审稿时长
>12 weeks
期刊介绍: Organogenesis is a peer-reviewed journal, available in print and online, that publishes significant advances on all aspects of organ development. The journal covers organogenesis in all multi-cellular organisms and also includes research into tissue engineering, artificial organs and organ substitutes. The overriding criteria for publication in Organogenesis are originality, scientific merit and general interest. The audience of the journal consists primarily of researchers and advanced students of anatomy, developmental biology and tissue engineering. The emphasis of the journal is on experimental papers (full-length and brief communications), but it will also publish reviews, hypotheses and commentaries. The Editors encourage the submission of addenda, which are essentially auto-commentaries on significant research recently published elsewhere with additional insights, new interpretations or speculations on a relevant topic. If you have interesting data or an original hypothesis about organ development or artificial organs, please send a pre-submission inquiry to the Editor-in-Chief. You will normally receive a reply within days. All manuscripts will be subjected to peer review, and accepted manuscripts will be posted to the electronic site of the journal immediately and will appear in print at the earliest opportunity thereafter.
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