Evidence map›Paper›PMID 27406916›Full record

ArticleScientific reports2016

Liver X receptor and STAT1 cooperate downstream of Gas6/Mer to induce anti-inflammatory arginase 2 expression in macrophages.

Si-Yoon Kim, Eun-Jin Lim, Young-So Yoon, Young-Ho Ahn, Eun-Mi Park, Hee-Sun Kim, Jihee Lee Kang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

33 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  9. Aberrant expressions of TAM receptors are associated with postoperative recurrence in chronic rhinosinusitis with nasal polyps.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2024
    Article
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  13. Review
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  15. mInternational journal of molecular sciences · 2022
    Article
  16. 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 1 country.

Si-Yoon KimDepartment of Physiology, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Eun-Jin LimTissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Young-So YoonDepartment of Physiology, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Young-Ho AhnTissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Eun-Mi ParkTissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Hee-Sun KimTissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Jihee Lee KangDepartment of Physiology, School of Medicine, Ewha Womans University, Seoul 158-710, Korea.
Ewha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mer signaling increases the transcriptional activity of liver X receptor (LXR) to promote the resolution of acute sterile inflammation. Here, we aimed to understand the pathway downstream of Mer signaling after growth arrest-specific protein 6 (Gas6) treatment that leads to LXR expression and transcriptional activity in mouse bone-marrow derived macrophages (BMDM). Gas6-induced increases in LXRα and LXRβ and expression of their target genes were inhibited in BMDM from STAT1(-/-) mice or by the STAT1-specific inhibitor fludarabine. Gas6-induced STAT1 phosphorylation, LXR activation, and LXR target gene expression were inhibited in BMDM from Mer(-/-) mice or by inhibition of PI3K or Akt. Gas6-induced Akt phosphorylation was inhibited in BMDM from STAT1(-/-) mice or in the presence of fludarabine. Gas6-induced LXR activity was enhanced through an interaction between LXRα and STAT1 on the DNA promoter of Arg2. Additionally, we found that Gas6 inhibited lipopolysaccharide (LPS)-induced nitrite production in a STAT1 and LXR pathway-dependent manner in BMDM. Additionally, Mer-neutralizing antibody reduced LXR and Arg2 expression in lung tissue and enhanced NO production in bronchoalveolar lavage fluid in LPS-induced acute lung injury. Our data suggest the possibility that the Gas6-Mer-PI3K/Akt-STAT1-LXR-Arg2 pathway plays an essential role for resolving inflammatory response in acute lung injury.

Indexed as

AnimalsArginaseBronchoalveolar Lavage FluidGrowth Arrest-Specific Protein 6InflammationIntercellular Signaling Peptides and ProteinsLiver X ReceptorsMacrophagesMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesPhosphorylationSignal TransductionSTAT1 Transcription FactorArg2 protein, mouseArginaseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsLiver X ReceptorsPhosphatidylinositol 3-KinasesStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID27406916
PMCPMC4942780
OpenAlexW2472529556

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Registered trials

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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.