Evidence map›Paper›PMID 25344066›Full record

Trial reportAmerican journal of physiology. Lung cellular and molecular physiology2014

Cigarette smoke enhances proliferation and extracellular matrix deposition by human fetal airway smooth muscle.

Elizabeth R Vogel, Sarah K VanOosten, Michelle A Holman, Danielle D Hohbein, Michael A Thompson, Robert Vassallo, Hitesh C Pandya, Y S Prakash, Christina M Pabelick

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report 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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Dysregulated iron metabolism in remodeling of aging asthmatic human airways.American journal of physiology. Cell physiology · 2026
    Article
  2. Smoking and endometriosis: A narrative review.Tobacco induced diseases · 2025
    Review
  3. Pharmacological therapy for stable chronic obstructive pulmonary disease.Chronic diseases and translational medicine · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Progress in the mechanism and targeted drug therapy for COPD.Signal transduction and targeted therapy · 2020
    Review
  11. TBK1 regulates YAP/TAZ and fibrogenic fibroblast activation.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  12. Review
  13. Differential estrogen-receptor activation regulates extracellular matrix deposition in human airway smooth muscle remodelingFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. Moderate hyperoxia induces senescence in developing human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  15. Hyperoxia-induced Cellular Senescence in Fetal Airway Smooth Muscle Cells.American journal of respiratory cell and molecular biology · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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.

Elizabeth R VogelDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota;
Sarah K VanOostenDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota;
Michelle A HolmanMayo Medical School, Rochester, Minnesota;
Danielle D HohbeinDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota;
Michael A ThompsonDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota;
Robert VassalloDepartment of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota; and.
Hitesh C PandyaDepartment of Pediatrics, University of Leicester, Leicester, United Kingdom.
Y S PrakashDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota;
Christina M PabelickDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota; Pabelick.christina@mayo.edu.
Mayo Clinic · USMayo Clinic in Arizona · USUniversity of Leicester · GB

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
NEURAL REGULATION OF AIRWAYS DURING POSTNATAL MATURATIONR01HL056470 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S. · 1996 to 2025
$10.5M
Neurotrophins in the LungR01HL088029 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S. · 2009 to 2022
$5.9M
Interdisciplinary Training in Lung Physiology and Biomedical EngineeringT32HL105355 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S., SIECK, GARY C. · 2012 to 2021
$3.9M
The Role of Caveolins in Lung InflammationR01HL090595 · NHLBI · MAYO CLINIC ROCHESTER · PI PABELICK, CHRISTINA MARIA · 2009 to 2013
$1.9M
NCATS NIH HHS UL1 TR000135NHLBI NIH HHS HL-056470NHLBI NIH HHS HL-090595NHLBI NIH HHS R01 HL056470NHLBI NIH HHS R01 HL088029NHLBI NIH HHS T32 HL105355NHLBI NIH HHS T3-HL-105355
6 · The paper itself

Abstract

Cigarette smoke is a common environmental insult associated with increased risk of developing airway diseases such as wheezing and asthma in neonates and children. In adults, asthma involves airway remodeling characterized by increased airway smooth muscle (ASM) cell proliferation and increased extracellular matrix (ECM) deposition, as well as airway hyperreactivity. The effects of cigarette smoke on remodeling and contractility in the developing airway are not well-elucidated. In this study, we used canalicular-stage (18-20 wk gestational age) human fetal airway smooth muscle (fASM) cells as an in vitro model of the immature airway. fASM cells were exposed to cigarette smoke extract (CSE; 0.5-1.5% for 24-72 h), and cell proliferation, ECM deposition, and intracellular calcium ([Ca(2+)]i) responses to agonist (histamine 10 μM) were used to evaluate effects on remodeling and hyperreactivity. CSE significantly increased cell proliferation and deposition of ECM molecules collagen I, collagen III, and fibronectin. In contrast, [Ca(2+)]i responses were not significantly affected by CSE. Analysis of key signaling pathways demonstrated significant increase in extracellular signal-related kinase (ERK) and p38 activation with CSE. Inhibition of ERK or p38 signaling prevented CSE-mediated changes in proliferation, whereas only ERK inhibition attenuated the CSE-mediated increase in ECM deposition. Overall, these results demonstrate that cigarette smoke may enhance remodeling in developing human ASM through hyperplasia and ECM production, thus contributing to development of neonatal and pediatric airway disease.

Indexed as

Cell ProliferationModels, BiologicalCalciumCalcium SignalingCollagen Type ICollagen Type IIIExtracellular MatrixFetusHumansMAP Kinase Signaling SystemMuscle, Smoothp38 Mitogen-Activated Protein KinasesRespiratory SystemSmokingCalciumCollagen Type ICollagen Type IIIp38 Mitogen-Activated Protein Kinasesasthmacollagenlung developmentprematurity

Identifiers

PMID25344066
PMCPMC4269688
OpenAlexW2167654458

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.