Evidence map›Paper›PMID 30729671›Full record

ArticleJournal of cellular and molecular medicine2019

The Pros1/Tyro3 axis protects against periodontitis by modulating STAT/SOCS signalling.

Lei Jiang, Xiao Qing Chen, Ming Jing Gao, Wai Lee, Jie Zhou, Yun Fu Zhao, Guo Dong Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Observational
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  7. The Role of TAM Receptors in Bone.International journal of molecular sciences · 2023
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  10. Armed to the Teeth-The Oral Mucosa Immunity System and Microbiota.International journal of molecular sciences · 2022
    Review
  11. Article
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  13. Article
  14. CD14Arthritis research & therapy · 2020
    Article
  15. Article
  16. Article
  17. 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 1 institution in 1 country.

Lei JiangDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Xiao Qing ChenDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Ming Jing GaoDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Wai LeeDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Jie ZhouDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Yun Fu ZhaoDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.
Guo Dong WangDepartment of Stomatology, Changzheng Hospital, Second Military Medical University, Shanghai, P. R. China.ORCID 0000-0002-6128-1286
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis, an oral inflammatory disease caused by periodontal pathogen infection, is the most prevalent chronic inflammatory disease and a major burden on healthcare. The TAM receptor tyrosine kinases (Tyro3, Axl and Mertk) and their ligands (Gas6 and Pros1) play a pivotal role in the resolution of inflammation and have been associated with chronic inflammatory and autoimmune diseases. In this study, we evaluated the effects of exogenous Pros1 in in vitro and in vivo models of periodontitis. We detected higher Pros1 but lower Tyro3 levels in inflamed gingival specimens of periodontitis patients compared with healthy controls. Moreover, Pros1 was mostly localized in the gingival epithelium of all specimens. In cultured human gingival epithelial cells (hGECs), Porphyromonas gingivalis LPS (p.g-LPS) stimulation down-regulated Pros1 and Tyro3. Exogenous Pros1 inhibited p.g-LPS-induced production of TNF-α, IL-6, IL-1β, MMP9/2 and RANKL in a Tyro3-dependent manner as revealed by PCR, Western blot analysis, ELISA and gelatin zymography. Pros1 also restored Tyro3 expression down-regulated by p.g-LPS in hGECs. In rats treated with ligature and p.g-LPS, administration of Pros1 attenuated periodontitis-associated gingival inflammation and alveolar bone loss. Our mechanistic studies implicated SOCS1/3 and STAT1/3 as mediators of the in vitro and in vivo anti-inflammatory effects of Pros1. Collectively, the findings from this work supported Pros1 as a novel anti-inflammatory therapy for periodontitis.

Indexed as

AdultAlveolar Bone LossAnimalsBacteroidaceae InfectionsCalcium-Binding ProteinsCase-Control StudiesDisease Models, AnimalFemaleGene Expression RegulationHumansLipopolysaccharidesMaleMiddle AgedPeriodontitisPorphyromonas gingivalisProtective AgentsCalcium-Binding ProteinsLipopolysaccharidesPROS1 protein, humanProtective AgentsProtein SReceptor Protein-Tyrosine KinasesSTAT1 protein, humanSTAT1 Transcription FactorSuppressor of Cytokine Signaling ProteinsTYRO3 protein, humanperiodontitisPros1SOCS1/3STAT1/3Tyro3

Identifiers

PMID30729671
PMCPMC6433735
OpenAlexW2914046742

What OpenQuestion holds

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LicenceCC BY
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.