Evidence map›Paper›PMID 32235405›Full record

ArticleInternational journal of molecular sciences2020

Expression and Role of IL-1β Signaling in Chondrocytes Associated with Retinoid Signaling during Fracture Healing.

Tsuyoshi Shimo, Hiroaki Takebe, Tatsuo Okui, Yuki Kunisada, Soichiro Ibaragi, Kyoichi Obata, Naito Kurio, Karnoon Shamsoon, Saki Fujii, Akihiro Hosoya and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Immunohistochemical Analysis of CCN2 in Experimental Fracture Healing Models.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  8. Article
  9. Article
  10. Molecular Processes in Chondrocyte Biology.International journal of molecular sciences · 2020
    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

13 authors at 5 institutions in 2 countries.

Tsuyoshi ShimoDivision of Reconstructive Surgery for Oral and Maxillofacial Region, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-0293, Japan.ORCID 0000-0002-7811-2366
Hiroaki TakebeDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-0293, Japan.
Tatsuo OkuiDepartments of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8525, Japan.ORCID 0000-0002-7640-3274
Yuki KunisadaDepartments of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8525, Japan.
Soichiro IbaragiDepartments of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8525, Japan.
Kyoichi ObataDepartments of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8525, Japan.
Naito KurioDepartment of Oral Surgery, Tokushima University Graduate School, Tokushima 770-8504, Japan.
Karnoon ShamsoonDivision of Clinical Cariology and Endodontology, Department of Oral Rehabilitation, School of Dentistry, University of Hokkaido, School of Dentistry, Hokkaido 061-0293, Japan.
Saki FujiiDivision of Reconstructive Surgery for Oral and Maxillofacial Region, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-0293, Japan.
Akihiro HosoyaDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-0293, Japan.
Kazuharu IrieDivision of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido 061-0293, Japan.
Akira SasakiDepartments of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8525, Japan.
Masahiro IwamotoDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Health Sciences University of Hokkaido · JPOkayama University · JPHokkaido University · JPTokushima University · JPUniversity of Maryland, Baltimore · US

Funding

Regulation of Skeletal Growth by Nuclear Retinoid ReceptorsR01AR056837 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI IWAMOTO, MASAHIRO, PACIFICI, MAURIZIO · 2009 to 2020
$3.4M
NIAMS NIH HHS R01 AR056837
6 · The paper itself

Abstract

The process of fracture healing consists of an inflammatory reaction and cartilage and bone tissue reconstruction. The inflammatory cytokine interleukin-1β (IL-1β) signal is an important major factor in fracture healing, whereas its relevance to retinoid receptor (an RAR inverse agonist, which promotes endochondral bone formation) remains unclear. Herein, we investigated the expressions of IL-1β and retinoic acid receptor gamma (RARγ) in a rat fracture model and the effects of IL-1β in the presence of one of several RAR inverse agonists on chondrocytes. An immunohistochemical analysis revealed that IL-1β and RARγ were expressed in chondrocytes at the fracture site in the rat ribs on day 7 post-fracture. In chondrogenic ATDC5 cells, IL-1β decreases the levels of aggrecan and type II collagen but significantly increased the metalloproteinase-13 (Mmp13) mRNA by real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. An RAR inverse agonist (AGN194310) inhibited IL-1β-stimulated Mmp13 and Ccn2 mRNA in a dose-dependent manner. Phosphorylated extracellular signal regulated-kinases (pERK1/2) and p-p38 mitogen-activated protein kinase (MAPK) were increased time-dependently by IL-1β treatment, and the IL-1β-induced p-p38 MAPK was inhibited by AGN194310. Experimental p38 inhibition led to a drop in the IL-1β-stimulated expressions of Mmp13 and Ccn2 mRNA. MMP13, CCN2, and p-p38 MAPK were expressed in hypertrophic chondrocytes near the invaded vascular endothelial cells. As a whole, these results point to role of the IL-1β via p38 MAPK as important signaling in the regulation of the endochondral bone formation in fracture healing, and to the actions of RAR inverse agonists as potentially relevant modulators of this process.

Indexed as

AnimalsBiomarkersChondrocytesFracture HealingGene ExpressionImmunohistochemistryInterleukin-1betaMaleMiceMitogen-Activated Protein KinasesModels, BiologicalProtein TransportRatsReceptors, Retinoic AcidRetinoidsSignal TransductionBiomarkersInterleukin-1betaMitogen-Activated Protein KinasesReceptors, Retinoic AcidRetinoidschondrocytefracture healinginterreukin-1βretinoid signaling

Identifiers

PMID32235405
PMCPMC7177407
OpenAlexW3013659466

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.