Evidence map›Paper›PMID 32267720›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020

Real-time measurement of cellular bioenergetics in fully differentiated human nasal epithelial cells grown at air-liquid-interface.

Emily Mavin, Bernard Verdon, Sean Carrie, Vinciane Saint-Criq, Jason Powell, Christian A Kuttruff, Chris Ward, James P Garnett, Satomi Miwa

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-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

14 citing papers in PubMed, 27 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

9 authors at 2 institutions in 2 countries.

Emily MavinInstitute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Bernard VerdonInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Sean CarrieInstitute of Health and Society, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Vinciane Saint-CriqInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Jason PowellInstitute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Christian A KuttruffMedicinal Chemistry, Boehringer Ingelheim Pharma, Biberach an der Riss, Germany.
Chris WardInstitute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.
James P GarnettInstitute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.ORCID 0000-0002-4767-020X
Satomi MiwaInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Newcastle University · GBBoehringer Ingelheim (Germany) · DE

Funding

Medical Research Council MC_PC_15030Medical Research Council MR/P020941/1MRF_ MRF-091-0001-RG-GARNE
6 · The paper itself

Abstract

Shifts in cellular metabolic phenotypes have the potential to cause disease-driving processes in respiratory disease. The respiratory epithelium is particularly susceptible to metabolic shifts in disease, but our understanding of these processes is limited by the incompatibility of the technology required to measure metabolism in real-time with the cell culture platforms used to generate differentiated respiratory epithelial cell types. Thus, to date, our understanding of respiratory epithelial metabolism has been restricted to that of basal epithelial cells in submerged culture, or via indirect end point metabolomics readouts in lung tissue. Here we present a novel methodology using the widely available Seahorse Analyzer platform to monitor real-time changes in the cellular metabolism of fully differentiated primary human airway epithelial cells grown at air-liquid interface (ALI). We show increased glycolytic, but not mitochondrial, ATP production rates in response to physiologically relevant increases in glucose availability. We also show that pharmacological inhibition of lactate dehydrogenase is able to reduce glucose-induced shifts toward aerobic glycolysis. This method is timely given the recent advances in our understanding of new respiratory epithelial subtypes that can only be observed in vitro through culture at ALI and will open new avenues to measure real-time metabolic changes in healthy and diseased respiratory epithelium, and in turn the potential for the development of novel therapeutics targeting metabolic-driven disease phenotypes.

Indexed as

AirCell DifferentiationComputer SystemsEnergy MetabolismAcidsCells, CulturedEpithelial CellsGlucoseHumansL-Lactate DehydrogenaseMetabolomicsNoseAcidsGlucoseL-Lactate Dehydrogenaseairway epitheliumglucosemetabolismSeahorse

Identifiers

PMID32267720
PMCPMC7347273
OpenAlexW3014481538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.