Evidence map›Paper›PMID 22281988›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Regulator of G-protein signaling-5 inhibits bronchial smooth muscle contraction in severe asthma.

Zhao Yang, Nariman Balenga, Philip R Cooper, Gautam Damera, Richard Edwards, Christopher E Brightling, Reynold A Panettieri, Kirk M Druey

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. RGS4 Overexpression in Lung Attenuates Airway Hyperresponsiveness in Mice.American journal of respiratory cell and molecular biology · 2018
    Article
  8. Orphan Adhesion GPCR GPR64/ADGRG2 Is Overexpressed in Parathyroid Tumors and Attenuates Calcium-Sensing Receptor-Mediated Signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017
    Article
  9. Article
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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

8 authors at 4 institutions in 2 countries.

Zhao YangMolecular Signal Transduction Section, Laboratory of Allergic Diseases, National Insitute of Allergy and Infectious Diseases/NIH, 10 Center Drive, Bethesda, MD 20982, USA. kdruey@niaid.nih.gov
Nariman Balenga
Philip R Cooper
Gautam Damera
Richard Edwards
Christopher E Brightling
Reynold A Panettieri
Kirk M Druey
University of Pennsylvania · USNational Institute of Allergy and Infectious Diseases · USUniversity of Leicester · GBNational Institutes of Health · US

Funding

Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZIAAI000939 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$7.3M
Regulation of Normal and Asthmatic Lung Function by G-Protein-Coupled ReceptorsZ01AI000939 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 2004 to 2008
$832k
Intramural NIH HHS Z01 AI000939NHLBI NIH HHS HL543102NHLBI NIH HHS HL544157NHLBI NIH HHS HL5452235NIEHS NIH HHS ES013505Wellcome Trust 082265
6 · The paper itself

Abstract

Severe asthma is associated with fixed airway obstruction attributable to inflammation, copious luminal mucus, and increased airway smooth muscle (ASM) mass. Paradoxically, studies demonstrated that the hypertrophic and hyperplastic ASM characteristic of severe asthma has reduced contractile capacity. We compared the G-protein-coupled receptor (GPCR)-induced Ca(2+) mobilization and expression of GPCRs and signaling proteins related to procontractile signaling in ASM derived postmortem from subjects who died of nonrespiratory causes, with cells from subjects who died of asthma. Despite the increased or comparable expression of contraction-promoting GPCRs (bradykinin B2 or histamine H1 and protease-activated receptor 1, respectively) in asthmatic ASM cells relative to cells from healthy donors, asthmatic ASM cells exhibited reduced histamine-induced Ca(2+) mobilization and comparable responses to bradykinin and thrombin, suggesting a postreceptor signaling defect. Accordingly, the expression of regulator of G-protein signaling-5 (RGS5), an inhibitor of ASM contraction, was increased in cultured, asthmatic ASM cells and in bronchial smooth muscle bundles of both human subjects with asthma and allergen-challenged mice, relative to those of healthy human subjects or naive mice. The overexpression of RGS5 impaired the release of Ca(2+) to thrombin, histamine, and carbachol, and reduced the contraction of precision-cut lung slices to carbachol. These results suggest that increased RGS5 expression contributes to decreased myocyte shortening in severe and fatal asthma.

Indexed as

Signal TransductionAdultAsthmaBronchiFemaleGTP-Binding ProteinsHumansMiddle AgedMuscle ContractionGTP-Binding Proteins

Identifiers

PMID22281988
PMCPMC3380291
OpenAlexW2037099932

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.