Evidence map›Paper›PMID 24838753›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Nicotine alters mucin rheological properties.

Eric Y Chen, Albert Sun, Chi-Shuo Chen, Alexander J Mintz, Wei-Chun Chin

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. Article
  5. Prolonged, physiologically relevant nicotine concentrations in the airways of smokers.American journal of physiology. Lung cellular and molecular physiology · 2023
    Observational
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Reliably sourced airway mucus.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Role of epithelial sodium channels in the regulation of lung fluid homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2015
    Review
  18. Article
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

5 authors at 2 institutions in 2 countries.

Eric Y ChenBioengineering, University of California at Merced, Merced, California; Center for Biomedical Engineering, Chang Gung University, Taoyuan, Taiwan; and MicroBase Technology Corporation, Taoyuan, Taiwan.
Albert SunBioengineering, University of California at Merced, Merced, California;
Chi-Shuo ChenBioengineering, University of California at Merced, Merced, California;
Alexander J MintzBioengineering, University of California at Merced, Merced, California;
Wei-Chun ChinBioengineering, University of California at Merced, Merced, California; wchin2@ucmerced.edu.
University of California, Merced · USChang Gung University · TW

Funding

Nicotine-induced mucin secretion in airway goblet cellsR15HL095039 · NHLBI · UNIVERSITY OF CALIFORNIA, MERCED · PI CHIN, WEI-CHUN · 2009 to 2009
$255k
NHLBI NIH HHS 1R15HL095039
6 · The paper itself

Abstract

Tobacco smoke exposure, the major cause of chronic obstructive pulmonary disease (COPD), instigates a dysfunctional clearance of thick obstructive mucus. However, the mechanism underlying the formation of abnormally viscous mucus remains elusive. We investigated whether nicotine can directly alter the rheological properties of mucin by examining its physicochemical interactions with human airway mucin gels secreted from A549 lung epithelial cells. Swelling kinetics and multiple particle tracking were utilized to assess mucin gel viscosity change when exposed to nicotine. Herein we show that nicotine (≤50 nM) significantly hindered postexocytotic swelling and hydration of released mucins, leading to higher viscosity, possibly by electrostatic and hydrophobic interactions. Moreover, the close association of nicotine and mucins allows airway mucus to function as a reservoir for prolonged nicotine release, leading to correlated pathogenic effects. Our results provide a novel explanation for the maltransport of poorly hydrated mucus in smokers. More importantly, this study further indicates that even low-concentration nicotine can profoundly increase mucus viscosity and thus highlights the health risks of secondhand smoke exposure.

Indexed as

AnimalsCells, CulturedEpithelial CellsGelsHumansMucinsMucusNicotineParticle SizeRheologySmokingSwineViscosityGelsMucinsNicotinechronic obstructive pulmonary diseaseenvironmental tobacco smokemucin swelling kineticsmucociliary clearancetobacco smokeviscosity

Identifiers

PMID24838753
PMCPMC4101795
OpenAlexW2325443543

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.