Evidence map›Paper›PMID 32303624›Full record

ArticleThorax2020

Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation.

Jennifer M Felton, David A Dorward, Jennifer A Cartwright, Philippe Md Potey, Calum T Robb, Jingang Gui, Ruth W Craig, Jürgen Schwarze, Christopher Haslett, Rodger Duffin and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Thorax, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 15 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

13 authors at 3 institutions in 2 countries.

Jennifer M FeltonUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0002-5004-0794
David A DorwardUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0002-4658-8829
Jennifer A CartwrightUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0003-1143-9011
Philippe Md PoteyUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.
Calum T RobbUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0002-0249-7212
Jingang GuiDepartment of Pharmacology and Toxicology, Dartmouth College Geisel School of Medicine, Hanover, New Hampshire, USA.
Ruth W CraigDepartment of Pharmacology and Toxicology, Dartmouth College Geisel School of Medicine, Hanover, New Hampshire, USA.
Jürgen SchwarzeUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0002-6899-748X
Christopher HaslettUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.
Rodger DuffinUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.
Ian DransfieldUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0001-5848-7059
Christopher D LucasUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK christopher.lucas@ed.ac.uk.ORCID 0000-0002-7523-0295
Adriano G RossiUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, UK.ORCID 0000-0003-3173-9521
Queen's Medical Centre · GBDartmouth College · USCincinnati Children's Hospital Medical Center · US

Funding

Medical Research Council G0800969Medical Research Council MR/K013386/1Wellcome Trust 206566/Z/17/Z
6 · The paper itself

Abstract

Eosinophils are key effector cells in allergic diseases. Here we investigated Mcl-1 (an anti-apoptotic protein) in experimental allergic airway inflammation using transgenic overexpressing human Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor. Overexpression of Mcl-1 exacerbated allergic airway inflammation, with increased bronchoalveolar lavage fluid cellularity, eosinophil numbers and total protein, and an increase in airway mucus production. Eosinophil apoptosis was suppressed by Mcl-1 overexpression, with this resistance to apoptosis attenuated by cyclin-dependent kinase inhibition which also rescued Mcl-1-exacerbated allergic airway inflammation. We propose that targeting Mcl-1 may be beneficial in treatment of allergic airway disease.

Indexed as

Gene Expression RegulationAnimalsApoptosisAsthmaBronchoalveolar Lavage FluidDisease Models, AnimalEosinophilsFemaleHypersensitivityLeukocyte CountMiceMice, TransgenicMyeloid Cell Leukemia Sequence 1 ProteinRNAMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 ProteinRNAallergic lung diseaseasthma mechanismseosinophil biology

Identifiers

PMID32303624
PMCPMC7361019
OpenAlexW3017303297

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.