Evidence map›Paper›PMID 26899203›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology

The ameloblastin extracellular matrix molecule enhances bone fracture resistance and promotes rapid bone fracture healing.

Xuanyu Lu, Wenjin Li, Satoshi Fukumoto, Yoshihiko Yamada, Carla A Evans, Tom Diekwisch, Xianghong Luan

Abstract read
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Ameloblastin and its multifunctionality in amelogenesis: A review.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Review
  4. Article
  5. Article
  6. The role of proteoglycan form of DMP1 in cranial repair.BMC molecular and cell biology · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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

7 authors at 4 institutions in 2 countries.

Xuanyu LuUniversity of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Oral Biology, United States; University of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Orthodontics, United States.
Wenjin LiDepartment of Prosthodontics, University of Shanxi, Shanxi, China.
Satoshi FukumotoCraniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, United States.
Yoshihiko YamadaCraniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, United States.
Carla A EvansUniversity of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Orthodontics, United States.
Tom DiekwischUniversity of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Oral Biology, United States; Texas A&M Baylor College of Dentistry, Department of Periodontics, United States. Electronic address: diekwisch@bcd.tamhsc.edu.
Xianghong LuanUniversity of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Oral Biology, United States; University of Illinois College of Dentistry, Brodie Laboratory for Craniofacial Genetics, Department of Orthodontics, United States. Electronic address: luan@uic.edu.
Illinois College · USNational Institutes of Health · USShanxi University · CNUniversity of Illinois Urbana-Champaign · US

Funding

Oral and Craniofacial Development and DiseaseZIADE000720 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, YOSHIHIKO · 2009 to 2017
$6.1M
Cartilage Development and DiseaseZIADE000483 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, YOSHIHIKO · 2009 to 2017
$5.9M
Ameloblastin Function in Periodontal DevelopmentR01DE019155 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LUAN, XIANGHONG · 2008 to 2012
$1.9M
BIOLOGY AND BIOMETRICS OF ENAMEL CRYSTAL GROWTHR01DE013378 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DIEKWISCH, THOMAS G.H. · 2001 to 2005
$1.3M
NIDCR NIH HHS R01 DE013378NIDCR NIH HHS R01 DE019155
6 · The paper itself

Abstract

The extracellular matrix (ECM) provides structural support, cell migration anchorage, cell differentiation cues, and fine-tuned cell proliferation signals during all stages of bone fracture healing, including cartilaginous callus formation, callus remodeling, and bony bridging of the fracture gap. In the present study we have defined the role of the extracellular matrix protein ameloblastin (AMBN) in fracture resistance and fracture healing of mouse long bones. To this end, long bones from WT and AMBN(Δ5-6) truncation model mice were subjected to biomechanical analysis, fracture healing assays, and stem cell colony formation comparisons. The effect of exogenous AMBN addition to fracture sites was also determined. Our data indicate that lack of a functional AMBN in the bone matrix resulted in 31% decreased femur bone mass and 40% reduced energy to failure. On a cellular level, AMBN function inhibition diminished the proliferative capacity of fracture repair callus cells, as evidenced by a 58% reduction in PCNA and a 40% reduction in Cyclin D1 gene expression, as well as PCNA immunohistochemistry. In terms of fracture healing, AMBN truncation was associated with an enhanced and prolonged chondrogenic phase, resulting in delayed mineralized tissue gene expression and delayed ossification of the fracture repair callus. Underscoring a role of AMBN in fracture healing, there was a 6.9-fold increase in AMBN expression at the fracture site one week after fracture, and distinct AMBN immunolabeling in the fracture gap. Finally, application of exogenous AMBN protein to bone fracture sites accelerated callus formation and bone fracture healing (33% increase in bone volume and 19% increase in bone mineral density), validating the findings of our AMBN loss of function studies. Together, these data demonstrate the functional importance of the AMBN extracellular matrix protein in bone fracture prevention and rapid fracture healing.

Indexed as

Fracture HealingAnimalsBiomechanical PhenomenaBony CallusCell DifferentiationDental Enamel ProteinsDisease Models, AnimalFemaleFemurFractures, BoneMaleMiceMutationAmbn protein, mouseDental Enamel ProteinsAmeloblastinBone fractureFracture healingMesenchymal stem cellsProliferation

Identifiers

PMID26899203
PMCPMC5651174
OpenAlexW2282924135

What OpenQuestion holds

Textmetadata
LicenceTDM
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.