Evidence map›Paper›PMID 22797250›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Severely blunted allergen-induced pulmonary Th2 cell response and lung hyperresponsiveness in type 1 transient receptor potential channel-deficient mice.

Eda Yildirim, Michelle A Carey, Jeffrey W Card, Alexander Dietrich, Gordon P Flake, Yingpei Zhang, J Alyce Bradbury, Yvette Rebolloso, Dori R Germolec, Daniel L Morgan and 2 more

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. From GTP and G proteins to TRPC channels: a personal account.Journal of molecular medicine (Berlin, Germany) · 2015
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. 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

12 authors at 3 institutions in 1 country.

Eda YildirimIntramural Research Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Michelle A Carey
Jeffrey W Card
Alexander Dietrich
Gordon P Flake
Yingpei Zhang
J Alyce Bradbury
Yvette Rebolloso
Dori R Germolec
Daniel L Morgan
Darryl C Zeldin
Lutz Birnbaumer
National Institutes of Health · USNational Institute of Environmental Health Sciences · USUniversity of California, Los Angeles · US

Funding

Alterations In Pulmonary Immune Function And Host Resistance In COX Null MiceZIAES025043 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 2009 to 2025
$11.7M
Investigation of Bronchiolitis Obliterans Caused by Diacetyl InhalationZIAES101865 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MORGAN, DANIEL · 2009 to 2015
$3.2M
Transmembrane Signaling Mechanisms Involving TRP ChannelsZIAES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2011 to 2014
$3.2M
Transmembrane Signaling Mechanisms Involving TRP ChannelsZ01ES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$2.1M
Alterations in pulmonary immune function &host resistanZ01ES025043 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 2000 to 2008
$1.3M
NIEHS NIH HHS ZO1-ES-025043NIEHS NIH HHS ZO1-ES-101684
6 · The paper itself

Abstract

Transient receptor potential channels (TRPCs) are widely expressed and regulate Ca²⁺ entry in the cells that participate in the pathophysiology of airway hyperreactivity, inflammation, and remodeling. In vitro studies point to a role for TRPC1-mediated Ca²⁺ signaling in several of these cell types; however, physiological evidence is lacking. Here we identify TRPC1 signaling as proinflammatory and a regulator of lung hyperresponsiveness during allergen-induced pulmonary response. TRPC1-deficient (Trpc1(-/-)) mice are hyposensitive to methacholine challenge and have significantly reduced allergen-induced pulmonary leukocyte infiltration coupled with an attenuated T helper type 2 (Th2) cell response. Upon in vitro allergen exposure, Trpc1(-/-) splenocytes show impaired proliferation and T cell receptor-induced IL-2 production. A high number of germinal centers in spleens of Trpc1(-/-) mice and elevated levels of immunoglobulins in their serum are indicative of dysregulated B cell function and homeostasis. Thus we propose that TRPC1 signaling is necessary in lymphocyte biology and in regulation of allergen-induced lung hyperresponsiveness, making TRPC1 a potential target for treatment of immune diseases and asthma.

Indexed as

AllergensAnimalsBronchial HyperreactivityFemaleInterleukin-2LungMaleMiceSignal TransductionSpleenTh2 CellsTRPC Cation ChannelsAllergensInterleukin-2transient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID22797250
PMCPMC3468476
OpenAlexW2153498873

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.