Evidence map›Paper›PMID 27088802›Full record

ArticleThe Journal of clinical investigation2016

Epithelium-generated neuropeptide Y induces smooth muscle contraction to promote airway hyperresponsiveness.

Shanru Li, Cynthia Koziol-White, Joseph Jude, Meiqi Jiang, Hengjiang Zhao, Gaoyuan Cao, Edwin Yoo, William Jester, Michael P Morley, Su Zhou and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Regulatory Peptides in Asthma.International journal of molecular sciences · 2021
    Review
  10. PAR-2-activated secretion by airway gland serous cells: role for CFTR and inhibition byAmerican journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Neuroimmune Pathophysiology in Asthma.Frontiers in cell and developmental biology · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

14 authors at 2 institutions in 2 countries.

Shanru Li
Cynthia Koziol-White
Joseph Jude
Meiqi Jiang
Hengjiang Zhao
Gaoyuan Cao
Edwin Yoo
William Jester
Michael P Morley
Su Zhou
Yi Wang
Min Min Lu
Reynold A Panettieri
Edward E Morrisey
Penn Center for AIDS Research · USCalifornia Institute for Regenerative Medicine · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Trevor M Penning · 2006 to 2026
$35.3M
Winged-helix repressors and lung developmentR01HL071589 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2003 to 2015
$4.6M
Epigenic Regulation of Lung Progenitor Repair and RegenerationU01HL110942 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MORRISEY, EDWARD E · 2012 to 2016
$3.4M
NHLBI NIH HHS R01 HL071589NHLBI NIH HHS U01 HL110942NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Asthma is one of the most common chronic diseases globally and can be divided into presenting with or without an immune response. Current therapies have little effect on nonimmune disease, and the mechanisms that drive this type of asthma are poorly understood. Here, we have shown that loss of the transcription factors forkhead box P1 (Foxp1) and Foxp4, which are critical for lung epithelial development, in the adult airway epithelium evokes a non-Th2 asthma phenotype that is characterized by airway hyperresponsiveness (AHR) without eosinophilic inflammation. Transcriptome analysis revealed that loss of Foxp1 and Foxp4 expression induces ectopic expression of neuropeptide Y (Npy), which has been reported to be present in the airways of asthma patients, but whose importance in disease pathogenesis remains unclear. Treatment of human lung airway explants with recombinant NPY increased airway contractility. Conversely, loss of Npy in Foxp1- and Foxp4-mutant airway epithelium rescued the AHR phenotype. We determined that NPY promotes AHR through the induction of Rho kinase activity and phosphorylation of myosin light chain, which induces airway smooth muscle contraction. Together, these studies highlight the importance of paracrine signals from the airway epithelium to the underlying smooth muscle to induce AHR and suggest that therapies targeting epithelial induction of this phenotype may prove useful in treatment of noneosinophilic asthma.

Indexed as

Muscle, SmoothAnimalsAsthmaForkhead Transcription FactorsHumansMiceMice, KnockoutMuscle ContractionMyosin Light ChainsNeuropeptide YRepressor ProteinsRespiratory Mucosarho-Associated KinasesForkhead Transcription FactorsFoxp1 protein, mouseFoxp4 protein, mouseMyosin Light ChainsNeuropeptide YRepressor Proteinsrho-Associated Kinases

Identifiers

PMID27088802
PMCPMC4855915
OpenAlexW2338929961

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.