期刊
DEVELOPMENTAL DYNAMICS
卷 251, 期 5, 页码 759-776出版社
WILEY
DOI: 10.1002/dvdy.436
关键词
mouse molar; RSDL; Shh signal; tooth regeneration; Wnt/beta-catenin
资金
- Open Subject Project of Fujian Provincial Oral Biomaterial Engineering Technology Research Center/Fujian Provincial Key Laboratory of Stomatology [2019kq07]
- Natural Science Foundation of Fujian Province, China [2019J02011]
The study showed that the Shh signaling pathway inhibitor effectively inhibited the expression of Shh signaling pathway components and promoted cell proliferation to revitalize the rudimentary successional dental lamina. Additionally, the formation of diphyodontic dentition may be related to up-regulation of FGF signal and the Sostdc1-Wnt negative feedback loop.
Background: Tooth regeneration depends on the longevity of the dental epithelial lamina. However, the exact mechanism of dental lamina regression has not yet been clarified. To explore the role of the Sonic hedgehog (Shh) signaling pathway in regression process of the rudimentary successional dental lamina (RSDL) in mice, we orally administered a single dose of a Shh signaling pathway inhibitor to pregnant mice between embryonic day 13.0 (E13.0) and E17.0. Results: We observed that the Shh signaling pathway inhibitor effectively inhibited the expression of Shh signaling pathway components and revitalized RSDL during E15.0-E17.0 by promoting cell proliferation. In addition, mRNA-seq, reverse transcription plus polymerase chain reaction (RT-qPCR), and immunohistochemical analyses indicated that diphyodontic dentition formation might be related to FGF signal up-regulation and the Sostdc1-Wnt negative feedback loop. Conclusions: Overall, our results indicated that the Shh signaling pathway may play an initial role in preventing further development of mouse RSDL in a time-dependent manner.
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