Evidence map›Paper›PMID 19371341›Full record

ArticleBritish journal of pharmacology2009

Transcriptional regulation of monocyte chemotactic protein-1 release by endothelin-1 in human airway smooth muscle cells involves NF-kappaB and AP-1.

Amy M Sutcliffe, Deborah L Clarke, Dawn A Bradbury, Lisa M Corbett, Jamie A Patel, Alan J Knox

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

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  7. Resvega Alleviates Hydroquinone-Induced Oxidative Stress in ARPE-19 Cells.International journal of molecular sciences · 2020
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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 3 institutions in 1 country.

Amy M SutcliffeNottingham Respiratory Biomedical Research Unit, University of Nottingham, City Hospital, Nottingham NG5 1PB, UK.
Deborah L Clarke
Dawn A Bradbury
Lisa M Corbett
Jamie A Patel
Alan J Knox
University of Nottingham · GBNottingham City Hospital · GBImperial College London · GB

Funding

British Heart FoundationWellcome Trust
6 · The paper itself

Abstract

background and purposeEndothelin-1 (ET-1) is implicated in airway inflammation in asthma, but the mechanisms of its effects are poorly understood. We studied the effect of ET-1 on expression of the chemokine, monocyte chemotactic protein-1 (MCP-1), in primary cultures of human airway smooth muscle cells. EXPERIMENTAL APPROACH: MCP-1 release was measured by elisa. Pharmacological antagonists/inhibitors, reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to study ET receptors and kinase cascades. Transcriptional regulation was studied by real-time RT-PCR, transient transfection studies and chromatin immunoprecipitation assay. Major findings were confirmed in cells from three donors and mechanistic studies in cells from one donor. KEY

resultsET-1 increased MCP-1 release through an ET(A) and ET(B) receptor-dependent mechanism. ET-1 increased MCP-1 mRNA levels but not mRNA stability suggesting it was acting transcriptionally. ET-1 increased the activity of an MCP-1 promoter-reporter construct. Serial deletions of the MCP-1 promoter mapped ET-1 effects to a region between -213 and -128 base pairs upstream of the translation start codon, containing consensus sequences for activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB). ET-1 promoted binding of AP-1 c-Jun subunit and NF-kappaB p65 subunit to the MCP-1 promoter. Blocking the inhibitor of kappaB kinase-2 with 2-[(aminocarbonyl)amino]-5-[4-fluorophenyl]-3-thiophenecarboxamide (TPCA-1) decreased ET-1-stimulated MCP-1 production. p38 and p44/p42 mitogen-activated protein kinases were involved in upstream signalling. CONCLUSIONS AND IMPLICATIONS: ET-1 regulated MCP-1 transcriptionally, via NF-kappaB and AP-1. The upstream signalling involved ET(A), ET(B) receptors, p38 and p44/p42 mitogen-activated protein kinases. These may be targets for novel asthma therapies.

Indexed as

Cells, CulturedChemokine CCL2Endothelin-1HumansJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocytes, Smooth MuscleNF-kappa Bp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptor, Endothelin AReceptor, Endothelin BRespiratory SystemSignal TransductionTranscription Factor AP-1CCL2 protein, humanChemokine CCL2Endothelin-1JNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa Bp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptor, Endothelin AReceptor, Endothelin BTranscription Factor AP-1

Identifiers

PMID19371341
PMCPMC2707990
OpenAlexW1846455015

What OpenQuestion holds

Textmetadata
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.