Evidence map›Paper›PMID 35195777›Full record

ArticleJournal of bone and mineral metabolism2022

p53 deficiency promotes bone regeneration by functional regulation of mesenchymal stromal cells and osteoblasts.

Toshimichi Nagashima, Tadashi Ninomiya, Yoshiki Nakamura, Shirabe Nishimura, Akiko Ohashi, Junya Aoki, Toshihide Mizoguchi, Morio Tonogi, Tomihisa Takahashi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bone and mineral metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 34% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

9 authors at 3 institutions in 1 country.

Toshimichi NagashimaDivision of Oral Structural and Functional Biology, Nihon University Graduate School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Tadashi NinomiyaDepartment of Anatomy, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan. ninomiya.tadashi@nihon-u.ac.jp.ORCID http://orcid.org/0000-0002-6302-2640
Yoshiki NakamuraDivision of Oral Structural and Functional Biology, Nihon University Graduate School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Shirabe NishimuraDivision of Oral Structural and Functional Biology, Nihon University Graduate School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Akiko OhashiDepartment of Anatomy, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Junya AokiDepartment of Oral and Maxillofacial Surgery, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Toshihide MizoguchiOral Health Science Center, Tokyo Dental College, 2-9-18 Kanda-Misaki-cho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Morio TonogiDepartment of Oral and Maxillofacial Surgery, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Tomihisa TakahashiDepartment of Anatomy, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan.
Nihon University · JPSurugadai Nihon University Hospital · JPTokyo Dental College · JP

Funding

Japan Society for the Promotion of Science JP18K09625Japan Society for the Promotion of Science JP20K09999Japan Society for the Promotion of Science JP20K18682
6 · The paper itself

Abstract

introductionThe detailed mechanism of the process during bone healing of drill-hole injury has been elucidated, but a crucial factor in regulating drill-hole healing has not been identified. The transcription factor p53 suppresses osteoblast differentiation through inhibition of osterix expression. In present study, we demonstrate the effects of p53 deficiency on the capacity of MSCs and osteoblasts during drill-hole healing. MATERIALS AND

methodsMesenchymal stromal cells (MSCs) and osteoblasts were collected from bone marrow and calvaria of p53 knockout (KO) mice, respectively. The activities of cell mobility, cell proliferation, osteoblast differentiation, and wound healing of MSCs and/or osteoblasts were determined by in vitro experiments. In addition, bone healing of drill-hole injury in KO mice was examined by micro-CT and immunohistological analysis using anti-osterix, Runx2, and sclerostin antibodies.

resultsKO MSCs stimulated cell mobility, cell proliferation, and osteoblast differentiation. Likewise, KO osteoblasts enhanced cell proliferation and wound healing. KO MSCs and osteoblasts showed high potency in the inflammation and callus formation phases compared to those from wild-type (WT) mice. In addition, increased expression of osterix and Runx2 was observed in KO MSCs and osteoblasts that migrated in the drill-hole. Conversely, sclerostin expression was inhibited in KO mice. Eventually, KO mice exhibited high repairability of drill-hole injury, suggesting a novel role of p53 in MSCs and osteoblasts in improving bone healing.

conclusionp53 Deficiency promotes bone healing of drill-hole injury by enhancing the bone-regenerative ability of MSCs and osteoblasts.

Indexed as

Bone RegenerationCore Binding Factor Alpha 1 SubunitMesenchymal Stem CellsOsteoblastsTumor Suppressor Protein p53AnimalsCell DifferentiationMiceMice, KnockoutOsteogenesisCore Binding Factor Alpha 1 SubunitTrp53 protein, mouseTumor Suppressor Protein p53Drill-hole healingMesenchymal stromal cellsOsteoblastsp53 deficiencySclerostin

Identifiers

PMID35195777
OpenAlexW4213457916

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.