Evidence map›Paper›PMID 20448051›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

Prenatal nicotine exposure increases GABA signaling and mucin expression in airway epithelium.

Xiao Wen Fu, Kelsey Wood, Eliot R Spindel

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Neuroimmune Pathophysiology in Asthma.Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. MIDD0301 - A first-in-class anti-inflammatory asthma drug targets GABABasic & clinical pharmacology & toxicology · 2019
    Article
  13. Article
  14. Review
  15. Pathophysiological Mechanisms of Asthma.Frontiers in pediatrics · 2019
    Review
  16. Article
  17. Review
  18. Early life allergen-induced mucus overproduction requires augmented neural stimulation of pulmonary neuroendocrine cell secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Xiao Wen FuDivision of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, 97006, USA.
Kelsey Wood
Eliot R Spindel
Oregon National Primate Research Center · US

Funding

Effect of Fetal Nicotine Exposure on Primate LungR01HL087710 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SPINDEL, ELIOT R · 2007 to 2011
$3.6M
NHLBI NIH HHS R01 HL087710
6 · The paper itself

Abstract

Maternal smoking during pregnancy increases the risk of respiratory disease in offspring, but surprisingly little is known about the underlying mechanisms. Nicotinic acetylcholine receptors (nAChRs) expressed in bronchial epithelial cells (BECs) mediate the effects of nicotine on lung development and function. Recently, BECs were also shown to express a GABAergic paracrine loop that was implicated in mucus overproduction in asthma. We therefore investigated the interactions between cholinergic and GABAergic signaling in rhesus macaque BECs, and found that nicotine upregulated GABA signaling in BECs through the sequential activation of BEC nAChR and GABA receptors. The incubation of primary cultures of rhesus BECs increased concentrations of GAD, GABA(A) receptors, and mucin mRNA. The nicotine-induced increase in glutamatic acid decarboxylase (GAD) and GABA(A) receptor mRNA resulted in increased GABA-induced currents and increased expression of mucin. The ability of nicotine to increase mucin expression was blocked by nicotinic and GABA(A) antagonists. These results implicate GABA signaling as a middleman in nicotine's effects on mucus overproduction. Similar effects of nicotine on GABA signaling and the expression of mucin were seen in vivo after chronic exposure of rhesus monkeys to nicotine. These data provide a new mechanism linking smoking with the increased mucin seen in asthma and chronic obstructive pulmonary disorder, and suggest a new paradigm of communication between non-neuronal transmitter systems in BECs. The existence of neural-like transmitter interactions in BECs suggests that some drugs active in the central nervous system may possess previously unexpected utility in respiratory diseases.

Indexed as

AnimalsBase SequenceBronchiCells, CulturedDNA PrimersEpithelial CellsFemalegamma-Aminobutyric AcidGlutamate DecarboxylaseHumansMacaca mulattaMucinsMucusNeurotransmitter AgentsNicotinePregnancyDNA Primersgamma-Aminobutyric AcidGlutamate DecarboxylaseMucinsNeurotransmitter AgentsNicotineReceptors, GABA-A

Identifiers

PMID20448051
PMCPMC3049233
OpenAlexW2159796677

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.