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논문 기본 정보

자료유형
학술저널
저자정보
Hwajung Choi (Chonbuk National University School of Dentistry) Tak-Heun Kim (Chonbuk National University School of Dentistry) Seung-O Ko (Chonbuk National University School of Dentistry) Eui-Sic Cho (Chonbuk National University School of Dentistry)
저널정보
대한치의학회 Journal of Korean Dental Science Journal of korean dental science Vol.9 No.1
발행연도
2016.6
수록면
9 - 18 (10page)

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Purpose: Wnt signaling plays an essential role in the dental epithelium and mesenchyme during tooth morphogenesis. Deletion of the Wntless (Wls) gene in odontoblasts appears to reduce canonical Wnt activity, leading to inhibition of odontoblast maturation. However, it remains unclear if autonomous Wnt ligands are necessary for differentiation of dental pulp cells into odontoblast-like cells to induce reparative dentinogenesis, one of well-known feature of pulp repair to form tertiary dentin.
Materials and Methods: To analyze the autonomous role of Wls for differentiation of dental pulp cells into odontoblast-like cells, we used primary dental pulp cells from unerupted molars of Wls-floxed allele mouse after infection with adenovirus for Cre recombinase expression to knockout the floxed Wls gene or control GFP expression. The differentiation of dental pulp cells into odontoblast-like cells was analyzed by quantitative real-time polymerase chain reaction.
Result: Proliferation rate was significantly decreased in dental pulp cells with Cre expression for Wls knockout. The expression levels of Osterix (Osx), runt-related transcription factor 2 (Runx2), and nuclear factor I-C (Nfic) were all significantly decreased by 0.3-fold, 0.2-fold, and 0.3-fold respectively in dental pulp cells with Wls knockout. In addition, the expression levels of Bsp, Col1a1, Opn, and Alpl were significantly decreased by 0.7-fold, 0.3-fold, 0.8-fold, and 0.6-fold respectively in dental pulp cells with Wls knockout.
Conclusion: Wnt ligands produced autonomously are necessary for proper proliferation and odontoblastic differentiation of mouse dental pulp cells toward further tertiary dentinogenesis.

목차

Introduction
Materials and Methods
Result
Discussion
Conclusion
References

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UCI(KEPA) : I410-ECN-0101-2017-515-000850390