Evidence map›Paper›PMID 29137360›Full record

ArticleOncotarget2017

Novel mechanisms for crotonaldehyde-induced lung edema.

Yue Li, Jianjun Chang, Yong Cui, Runzhen Zhao, Yan Ding, Yapeng Hou, Zhiyu Zhou, Hong-Long Ji, Hongguang Nie

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 24 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 3 institutions in 2 countries.

Yue Li *Institute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
Jianjun Chang *Institute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
Yong CuiDepartment of Anesthesiology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Runzhen ZhaoDepartment of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, Texas 75708, USA.
Yan DingInstitute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
Yapeng HouInstitute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
Zhiyu ZhouInstitute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
Hong-Long JiDepartment of Cellular and Molecular Biology, University of Texas Health Science Center at Tyler, Tyler, Texas 75708, USA.
Hongguang NieInstitute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang 110122, Liaoning, China.
China Medical University · CNThe University of Texas Health Science Center at Tyler · USFirst Hospital of China Medical University · CN

Funding

Regulation of lung epithelial sodium channels by cGMPR01HL087017 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI JI, HONG-LONG · 2007 to 2011
$1.6M
ENaC Expression in Human COPD Airway and Lung TissuesR03HL095435 · NHLBI · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI JI, HONG-LONG · 2009 to 2009
$71k
NHLBI NIH HHS R01 HL087017NHLBI NIH HHS R03 HL095435
6 · The paper itself

Abstract

backgroundCrotonaldehyde is a highly noxious α,β-unsaturated aldehyde in cigarette smoke that causes edematous acute lung injury.

objectiveTo understand how crotonaldehyde impairs lung function, we examined its effects on human epithelial sodium channels (ENaC), which are major contributors to alveolar fluid clearance.

methodsWe studied alveolar fluid clearance in C57 mice and ENaC activity was examined in H441 cells. Expression of α- and γ-ENaC was measured at protein and mRNA levels by western blot and real-time PCR, respectively. Intracellular ROS levels were detected by the dichlorofluorescein assay. Heterologous αβγ-ENaC activity was observed in an oocyte model.

resultsOur results showed that crotonaldehyde reduced transalveolar fluid clearance in mice. Furthermore, ENaC activity in H441 cells was inhibited by crotonaldehyde dose-dependently. Expression of α- and γ-subunits of ENaC was decreased at the protein and mRNA level in H441 cells exposed to crotonaldehyde, which was probably mediated by the increase in phosphorylated extracellular signal-regulated protein kinases 1 and 2. ROS levels increased time-dependently in cells exposed to crotonaldehyde. Heterologous αβγ-ENaC activity was rapidly eliminated by crotonaldehyde.

conclusionOur findings suggest that crotonaldehyde causes edematous acute lung injury by eliminating ENaC activity at least partly via facilitating the phosphorylation of extracellular signal-regulated protein kinases 1 and 2 signal molecules. Long-term exposure may decrease the expression of ENaC subunits and damage the cell membrane integrity, as well as increase the levels of cellular ROS products.

Indexed as

alveolar fluid clearancecrotonaldehydeepithelial sodium channelslung injuryreactive oxygen species

Identifiers

PMID29137360
PMCPMC5663532
OpenAlexW2613126668

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.