Evidence map›Paper›PMID 22155782›Full record

ArticleMolecular pharmacology2012

Transient receptor potential vanilloid-1 (TRPV1) is a mediator of lung toxicity for coal fly ash particulate material.

Cassandra E Deering-Rice, Mark E Johansen, Jessica K Roberts, Karen C Thomas, Erin G Romero, Jeewoo Lee, Garold S Yost, John M Veranth, Christopher A Reilly

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Epidemiological and mechanistic links between PMFrontiers in endocrinology · 2025
    Pooled it
  2. Modulation of TRPV-1 by prostaglandin-EScientific reports · 2020
    Trial
  3. In vivo human time-exposure study of orally dosed commercial silver nanoparticles.Nanomedicine : nanotechnology, biology, and medicine · 2014
    Trial
  4. Article
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  12. Review
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  14. Review
  15. Article
  16. TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021
    Review
  17. Effect ofJournal of personalized medicine · 2021
    Article
  18. Review
  19. Article
  20. Air Pollution-Induced Autonomic Modulation.Physiology (Bethesda, Md.) · 2020
    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 2 institutions in 2 countries.

Cassandra E Deering-RiceDepartment of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah 84112, USA.
Mark E Johansen
Jessica K Roberts
Karen C Thomas
Erin G Romero
Jeewoo Lee
Garold S Yost
John M Veranth
Christopher A Reilly
University of Utah · USSeoul National University · KR

Funding

TRP Channels and Air PollutionR01ES017431 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2009 to 2024
$5.3M
NIEHS NIH HHS ES017431NIEHS NIH HHS R01 ES017431
6 · The paper itself

Abstract

Environmental particulate matter (PM) pollutants adversely affect human health, but the molecular basis is poorly understood. The ion channel transient receptor potential vanilloid-1 (TRPV1) has been implicated as a sensor for environmental PM and a mediator of adverse events in the respiratory tract. The objectives of this study were to determine whether TRPV1 can distinguish chemically and physically unique PM that represents important sources of air pollution; to elucidate the molecular basis of TRPV1 activation by PM; and to ascertain the contributions of TRPV1 to human lung cell and mouse lung tissue responses exposed to an insoluble PM agonist, coal fly ash (CFA1). The major findings of this study are that TRPV1 is activated by some, but not all of the prototype PM materials evaluated, with rank-ordered responses of CFA1 > diesel exhaust PM > crystalline silica; TRP melastatin-8 is also robustly activated by CFA1, whereas other TRP channels expressed by airway sensory neurons and lung epithelial cells that may also be activated by CFA1, including TRPs ankyrin 1 (A1), canonical 4α (C4α), M2, V2, V3, and V4, were either slightly (TRPA1) or not activated by CFA1; activation of TRPV1 by CFA1 occurs via cell surface interactions between the solid components of CFA1 and specific amino acid residues of TRPV1 that are localized in the putative pore-loop region; and activation of TRPV1 by CFA1 is not exclusive in mouse lungs but represents a pathway by which CFA1 affects the expression of selected genes in lung epithelial cells and airway tissue.

Indexed as

Base SequenceCell Line, TransformedCoal AshDNA PrimersGene Expression ProfilingHumansLungPolymerase Chain ReactionTRPV Cation ChannelsCoal AshDNA PrimersTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID22155782
PMCPMC3286291
OpenAlexW2082071469

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.