Evidence map›Paper›PMID 26644796›Full record

ArticleAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology2015

TNF up-regulates Pentraxin3 expression in human airway smooth muscle cells via JNK and ERK1/2 MAPK pathways.

Jingbo Zhang, Latifa Koussih, Lianyu Shan, Andrew J Halayko, Ben-Kuen Chen, Abdelilah S Gounni

Open access · goldAbstract read
In one paragraph

Article in Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology, 2015. 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
1.1field-weighted citation impact, top 23% 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, 29 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Jingbo ZhangDepartment of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada ; Department of Nephrology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037 China.
Latifa KoussihDepartment of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada ; Universite de Saint Boniface, 200 Avenue de la cathedrale, Winnipeg, MB Canada.
Lianyu ShanDepartment of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada.
Andrew J HalaykoDepartment of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada ; Physiology and Physiopathology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada.
Ben-Kuen ChenInstitute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Abdelilah S GounniDepartment of Immunology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB Canada.
University of Manitoba · CANational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong pentraxin 3 (PTX3) is a novel candidate marker for inflammation in many chronic diseases. As a soluble pattern recognition receptor, PTX3 is involved in amplification of inflammatory reactions and regulation of innate immunity. Previously, we demonstrate that human airway smooth muscle cells (HASMC) express constitutively PTX3 and upon TNF stimulation. However, very little is known about the mechanism governing its expression in HASMC. We sought to investigate the mechanism governing TNF induced PTX3 expression in primary HASMC.

methodsHASMC were stimulated with TNF in the presence of transcriptional inhibitor actinomycin D (ActD) or MAPKs pharmacological inhibitors. PTX3 mRNA and protein expression were analyzed by Real-time RT-PCR and ELISA, respectively. PTX3 promoter activity was determined using luciferase assay.

resultsPTX3 mRNA and protein are expressed constitutively by HASMC and significantly up-regulated by TNF. TNF-induced PTX3 mRNA and protein release in HASMC were inhibited by transcriptional inhibitor actinomycin D. TNF induced significantly PTX3 promoter activation in HASMC. MAPK JNK and ERK1/2 specific inhibitors (SP600125 and UO126), but not p38, significantly down regulates TNF induced PTX3 promoter activity and protein release in HASMC. Finally, TNF mediated PTX3 promoter activity in HASMC was abolished upon mutation of NF-κβ and AP1 binding sites.

conclusionsOur data suggest that TNF induced PTX3 in HASMC at least via a transcriptional mechanism that involved MAPK (JNK and ERK1/2), NF-κβ and AP1 pathways. These results rise the possibility that HASMC derived PTX3 may participate in immune regulation in the airways.

Indexed as

Airway smooth muscle cellsPentraxin-3SignalingTNF

Identifiers

PMID26644796
PMCPMC4671218
OpenAlexW2182389352

What OpenQuestion holds

Textmetadata
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.