Evidence map›Paper›PMID 32462812›Full record

ArticleJournal of cellular and molecular medicine2020

Crosstalk between Akt and NF-κB pathway mediates inhibitory effect of gas6 on monocytes-endothelial cells interactions stimulated by P. gingivalis-LPS.

Xuekui Wang, Yingjun Liu, Shengnan Zhang, Xiangying Ouyang, Yuguang Wang, Yong Jiang, Na An

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  6. Article
  7. Article
  8. Review
  9. Review
  10. The Roles of Periodontal Bacteria in Atherosclerosis.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Frontiers in immunology · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. 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

7 authors at 1 institution in 2 countries.

Xuekui WangDepartment of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing, China.
Yingjun LiuDepartment of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing, China.
Shengnan ZhangDepartment of Periodontology, Peking University School and Hospital of Stomatology, Beijing, China.
Xiangying OuyangDepartment of Periodontology, Peking University School and Hospital of Stomatology, Beijing, China.
Yuguang WangNational Engineering Laboratory for Digital and Material Technology of Stomatology, Peking University School and Hospital of Stomatology, Beijing, China.
Yong JiangDepartment of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing, China.
Na AnDepartment of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing, China.ORCID 0000-0001-8569-2437
King University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Correlation between periodontitis and atherosclerosis is well established, and the inherent mechanisms responsible for this relationship remain unclear. The biological function of growth arrest-specific 6 (gas6) has been discovered in both atherosclerosis and inflammation. Inhibitory effects of gas6 on the expression of inflammatory factors in human umbilical vein endothelial cells (HUVECs) stimulated by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis-LPS) were reported in our previous research. Herein, the effects of gas6 on monocytes-endothelial cells interactions in vitro and their probable mechanisms were further investigated. Gas6 protein in HUVECs was knocked down with siRNA or overexpressed with plasmids. Transwell inserts and co-culturing system were introduced to observe chemotaxis and adhering affinity between monocytes and endothelial cells in vitro. Expression of gas6 was decreased in inflammatory periodontal tissues and HUVECs challenged with P. gingivalis-LPS. The inhibitory effect of gas6 on chemotaxis and adhesion affinity between monocytes and endothelial cells was observed, and gas6 promoted Akt phosphorylation and inhibited NF-κB phosphorylation. To our best knowledge, we are first to report that gas6 inhibit monocytes-endothelial cells interactions in vitro induced by P. gingivalis-LPS via Akt/NF-κB pathway. Additionally, inflammation-mediated inhibition of gas6 expression is through LncRNA GAS6-AS2, rather than GAS6-AS1, which is also newly reported.

Indexed as

Cell CommunicationSignal TransductionAxl Receptor Tyrosine KinaseCell AdhesionCells, CulturedChemotaxis, Leukocytec-Mer Tyrosine KinaseEndothelial CellsGene ExpressionGrowth Arrest-Specific Protein 6HumansHuman Umbilical Vein Endothelial CellsIntercellular Signaling Peptides and ProteinsLipopolysaccharidesMonocytesNF-kappa BAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsLipopolysaccharidesMERTK protein, humanNF-kappa BProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor Protein-Tyrosine Kinasesendothelial cellsgas6GAS6-AS2lipopolysaccharidePorphyromonas gingivalis

Identifiers

PMID32462812
PMCPMC7348146
OpenAlexW3030019417

What OpenQuestion holds

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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.