Evidence map›Paper›PMID 31059030›Full record

ArticleMolecular medicine reports2019

Interleukin‑17A facilitates osteoclast differentiation and bone resorption via activation of autophagy in mouse bone marrow macrophages.

Lu Song, Jingyi Tan, Zhongxiu Wang, Peihui Ding, Qi Tang, Mengjiao Xia, Yingming Wei, Lili Chen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  17. Long-term implications of COVID-19 on bone health: pathophysiology and therapeutics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Lu SongDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Jingyi TanDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Zhongxiu WangDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Peihui DingDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Qi TangDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Mengjiao XiaDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Yingming WeiDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Lili ChenDepartment of Periodontology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 17A (IL‑17A) exerts pleiotropic effects on periodontitis, partially through enhancement of alveolar bone loss. Osteoclasts are the main culprits that absorb alveolar bone. However, studies describing the correlation between IL‑17A and osteoclasts are not conclusive. Previously, autophagy was revealed to be involved in osteoclast differentiation and bone resorption. However, the role of autophagy in IL‑17A‑mediated osteoclast formation is yet to be clarified. In the present study, bone marrow macrophages (BMMs) were treated with or without IL‑17A. 3‑Methyladenine (3‑MA) was applied to inhibit autophagy. Osteoclast formation was detected by tartrate‑resistant acid phosphatase (TRAP) staining, immunofluorescence, and scanning electron microscope. The effects of IL‑17A on osteoclast‑specific genes and autophagy‑related genes during osteoclast differentiation were examined by real‑time quantitative polymerase chain reaction and western blot analysis. Autophagosomes were observed by transmission electron microscope. Hematoxylin and eosin (H&E), and TRAP staining was adopted to assess alveolar bone destruction and the number of osteoclasts, respectively in a rat periodontitis model. Consequently, IL‑17A stimulated osteoclast differentiation and bone resorption of BMMs accompanied by an increase in the mRNA expression of osteoclast‑specific genes. Furthermore, IL‑17A increased the levels of autophagy‑related genes and proteins, and inhibition of autophagy with 3‑MA attenuated the IL‑17A‑mediated osteoclastogenesis. In addition, there was an increase in the number of osteoclasts and alveolar bone resorption with IL‑17A treatment in the periodontitis rat model. Collectively, these findings indicated that IL‑17A facilitated osteoclast differentiation and bone resorption in vitro and in vivo, which may contribute to the understanding of the molecular basis of IL‑17A in alveolar bone destruction and provide insight on the clinical therapeutic targets for periodontitis.

Indexed as

ActinsAdenineAlveolar Bone LossAnimalsAutophagosomesAutophagyBone MarrowBone ResorptionCell DifferentiationCell SurvivalDisease Models, AnimalFemaleGene Expression RegulationImmunohistochemistryInterleukin-17Macrophages3-methyladenineActinsAdenineInterleukin-17

Identifiers

PMID31059030
PMCPMC6522800
OpenAlexW2939670601

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.