Evidence map›Paper›PMID 39589557›Full record

ArticleHistochemistry and cell biology2024

Polycomb protein Bmi1 promotes odontoblast differentiation by accelerating Wnt and BMP signaling pathways.

Akihiro Hosoya, Hiroaki Takebe, Yuri Seki-Kishimoto, Yukiko Noguchi, Tadashi Ninomiya, Akira Yukita, Nagako Yoshiba, Ayako Washio, Masahiro Iijima, Takahiko Morotomi and 2 more

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Article in Histochemistry and cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Akihiro HosoyaDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, 061-0293, Japan. hosoya@hoku-iryo-u.ac.jp.
Hiroaki TakebeDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, 061-0293, Japan.
Yuri Seki-KishimotoDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, 061-0293, Japan.
Yukiko NoguchiDivision of Orthodontics and Dentofacial Orthopedics, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, Japan.
Tadashi NinomiyaDepartment of Anatomy, Nihon University School of Dentistry, Tokyo, Japan.
Akira YukitaFaculty of Education, Shizuoka University, Shizuoka, Japan.
Nagako YoshibaDepartment of Oral Health Science, Course for Oral Life Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Ayako WashioDivision of Endodontics and Restorative Dentistry, Department of Oral Functions, Kyushu Dental University, Fukuoka, Japan.
Masahiro IijimaDivision of Orthodontics and Dentofacial Orthopedics, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, Japan.
Takahiko MorotomiDepartment of Endodontics, School of Dentistry, Aichi Gakuin University, Aichi, Japan.
Chiaki KitamuraDivision of Endodontics and Restorative Dentistry, Department of Oral Functions, Kyushu Dental University, Fukuoka, Japan.
Hiroaki NakamuraInstitute for Oral Science, Matsumoto Dental University, Nagano, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bmi1 is a polycomb protein localized in stem cells and maintains their stemness. This protein is also reported to regulate the expression of various differentiation genes. In this study, to analyze the role of Bmi1 during dentinogenesis, we examined the immunohistochemical localization of Bmi1 during rat tooth development as well as after cavity preparation. Bmi1 localization was hardly detected in the dental mesenchyme at the bud and cap stages. After the bell stage, however, this protein became detectable in preodontoblasts and early odontoblasts just beginning dentin matrix secretion. As dentin formation progressed, Bmi1 immunoreactivity in the odontoblasts decreased in intensity. After cavity preparation, cells lining the dentin and some pulp cells under the cavity were immunopositive for Bmi1 at 4 days. Odontoblast-like cells forming reparative dentin were immunopositive for Bmi1 at 1 week, whereas their immunoreactivity was not detected after 8 weeks. We further analyzed the function of Bmi1 using KN-3 cells, a dental mesenchymal cell line. Overexpression of Bmi1 in KN-3 cells promoted mineralized tissue formation. In contrast, siRNA knockdown of Bmi1 in KN-3 cells reduced alkaline phosphatase activity and the expression of odontoblast differentiation marker genes such as Runx2, osterix, and osteocalcin. Additionally, KN-3 cells transfected with siRNA against Bmi1 showed reduced nuclear transition of β-catenin and expression of phosphorylated-Smad1/5/8. Taken together, these findings suggest that Bmi1 was localized in the odontoblast-lineage cells in their early differentiation stages. Bmi1 might positively regulate their differentiation by accelerating Wnt and BMP signaling pathways.

Indexed as

Bone Morphogenetic ProteinsCell DifferentiationOdontoblastsPolycomb Repressive Complex 1Signal TransductionAnimalsCells, CulturedRatsWnt ProteinsWnt Signaling PathwayBone Morphogenetic ProteinsPolycomb Repressive Complex 1Wnt ProteinsBmi1Dentin formationOdontoblast differentiationPolycomb proteinReparative dentin

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.