Evidence map›Paper›PMID 28714001›Full record

ArticleMolecular medicine reports2017

LPS enhances TLR4 expression and IFN‑γ production via the TLR4/IRAK/NF‑κB signaling pathway in rat pulmonary arterial smooth muscle cells.

Pengyan Wang, Xuhui Han, Biwen Mo, Guojin Huang, Changming Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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    Review
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  19. Malnutrition, poor post-natal growth, intestinal dysbiosis and the developing lung.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Review
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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

5 authors at 1 institution in 1 country.

Pengyan WangDivision of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
Xuhui HanDivision of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
Biwen MoDivision of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
Guojin HuangDivision of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
Changming WangDivision of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
Guilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the role of the Toll‑like receptor (TLR)4 signaling pathway in cellular response to lipopolysaccharide (LPS) in rat pulmonary artery smooth muscle cells (PASMCs). Chronic obstructive pulmonary disease (COPD) rats were established with passive inhaling cigarette smoke plus injection of LPS. The TLR4 protein in lung tissues was determined with immunohistochemical staining and protein levels of the components of the TLR4 pathway in PASMCs were analyzed with western blotting. The production of interferon (IFN)‑γ upon LPS stimulation in PASMCs was measured with ELISA. TLR4 expression in lung tissue from COPD rats was increased obviously compared with that in normal group. LPS enhances TLR4 expression in rat PASMCs and induced production of IFN‑γ dramatically. LPS treatment resulted in increased phosphor‑interleukin‑1 receptor‑associated kinase (IRAK), IκB and IκB kinase, as well as the total protein of nuclear factor (NF)‑κB p65. TLR4 inhibitor TAK‑242, IRAK1/4 inhibitor and NF‑κB inhibitor Bay 117082 were capable of suppressing the effects of LPS. TLR4 signaling pathway is functional in PASMCs, and may be involved in the inflammatory response during the pathogenesis of COPD.

Indexed as

AnimalsFemaleInterferon-gammaInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesLungMaleMyocytes, Smooth MuscleNF-kappa BNitrilesPulmonary ArteryPulmonary Disease, Chronic ObstructiveRats, WistarSignal TransductionSulfonamidesSulfones3-(4-methylphenylsulfonyl)-2-propenenitrileethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateInterferon-gammaInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesNF-kappa BNitrilesSulfonamidesSulfonesToll-Like Receptor 4

Identifiers

PMID28714001
PMCPMC5547977
OpenAlexW2734346863

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.