Evidence map›Paper›PMID 24957904›Full record

ArticleRespiratory research2014

Accumulation of metals in GOLD4 COPD lungs is associated with decreased CFTR levels.

Fatemat Hassan, Xiaohua Xu, Gerard Nuovo, David W Killilea, Jean Tyrrell, Chong Da Tan, Robert Tarran, Philip Diaz, Junbae Jee, Daren Knoell and 2 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

48 citing papers in PubMed, 65 citations in OpenAlex.

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  17. Targeting the EGFR-ERK axis using the compatible solute ectoine to stabilize CFTR mutant F508del.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  18. Article
  19. Environmental Substances Associated with Chronic Obstructive Pulmonary Disease-A Scoping Review.International journal of environmental research and public health · 2022
    Article
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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

12 authors at 4 institutions in 1 country.

Fatemat Hassan
Xiaohua Xu
Gerard Nuovo
David W Killilea
Jean Tyrrell
Chong Da Tan
Robert Tarran
Philip Diaz
Junbae Jee
Daren Knoell
Prosper N Boyaka
Estelle Cormet-BoyakaDepartment of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA. boyaka.2@osu.edu.
The Ohio State University · USUniversity of North Carolina at Chapel Hill · USBrookdale University Hospital and Medical Center · USPhylogeny (United States) · US

Funding

The Impact of Tobacco Exposure on the Lungs Innate Defense SystemP50HL120100 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RANDELL, SCOTT H · 2013 to 2017
$21.0M
SPLUNC1-Derived Peptides as ENaC AntagonistsR01HL108927 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TARRAN, ROBERT · 2012 to 2015
$1.4M
Toxic metals and ion channels in cigarette-smoke induced COPDR03HL095442 · NHLBI · OHIO STATE UNIVERSITY · PI CORMET-BOYAKA, ESTELLE A · 2009 to 2010
$150k
NHLBI NIH HHS HL095442NHLBI NIH HHS HL108927NHLBI NIH HHS P50 HL120100NHLBI NIH HHS R01 HL108927
6 · The paper itself

Abstract

backgroundThe Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a chloride channel that primarily resides in airway epithelial cells. Decreased CFTR expression and/or function lead to impaired airway surface liquid (ASL) volume homeostasis, resulting in accumulation of mucus, reduced clearance of bacteria, and chronic infection and inflammation.

methodsExpression of CFTR and the cigarette smoke metal content were assessed in lung samples of controls and COPD patients with established GOLD stage 4. CFTR protein and mRNA were quantified by immunohistochemistry and quantitative RT-PCR, respectively. Metals present in lung samples were quantified by ICP-AES. The effect of cigarette smoke on down-regulation of CFTR expression and function was assessed using primary human airway epithelial cells. The role of leading metal(s) found in lung samples of GOLD 4 COPD patients involved in the alteration of CFTR was confirmed by exposing human bronchial epithelial cells 16HBE14o- to metal-depleted cigarette smoke extracts.

resultsWe found that CFTR expression is reduced in the lungs of GOLD 4 COPD patients, especially in bronchial epithelial cells. Assessment of metals present in lung samples revealed that cadmium and manganese were significantly higher in GOLD 4 COPD patients when compared to control smokers (GOLD 0). Primary human airway epithelial cells exposed to cigarette smoke resulted in decreased expression of CFTR protein and reduced airway surface liquid height. 16HBE14o-cells exposed to cigarette smoke also exhibited reduced levels of CFTR protein and mRNA. Removal and/or addition of metals to cigarette smoke extracts before exposure established their role in decrease of CFTR in airway epithelial cells.

conclusionsCFTR expression is reduced in the lungs of patients with severe COPD. This effect is associated with the accumulation of cadmium and manganese suggesting a role for these metals in the pathogenesis of COPD.

Indexed as

AgedCells, CulturedCystic Fibrosis Transmembrane Conductance RegulatorFemaleHumansLungMaleMetals, HeavyMiddle AgedPulmonary Disease, Chronic ObstructiveRespiratory MucosaSmokeTobacco ProductsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorMetals, HeavySmoke

Identifiers

PMID24957904
PMCPMC4106203
OpenAlexW2115111949

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.