Evidence map›Paper›PMID 32938721›Full record

ArticleMolecular pharmacology2020

Transient Receptor Potential Ankyrin-1 and Vanilloid-3 Differentially Regulate Endoplasmic Reticulum Stress and Cytotoxicity in Human Lung Epithelial Cells After Pneumotoxic Wood Smoke Particle Exposure.

Nam D Nguyen, Tosifa A Memon, Katherine L Burrell, Marysol Almestica-Roberts, Emmanuel Rapp, Lili Sun, Abigail F Scott, Joseph E Rower, Cassandra E Deering-Rice, Christopher A Reilly

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2020. 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
0.8field-weighted citation impact, top 28% 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, 18 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. CYP1B1 modulates stress and repair pathways in airway cells challenged by wood smoke particles.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  4. The role of TRPA1 in lung cancer.Translational lung cancer research · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. New Frontiers on ER Stress Modulation: Are TRP Channels the Leading Actors?International journal of molecular sciences · 2022
    Review
  15. Article
  16. TRP Channels as Cellular Targets of Particulate Matter.International journal of molecular sciences · 2021
    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

10 authors at 1 institution in 1 country.

Nam D NguyenDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Tosifa A MemonDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Katherine L BurrellDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Marysol Almestica-RobertsDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Emmanuel RappDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Lili SunDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Abigail F ScottDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Joseph E RowerDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Cassandra E Deering-RiceDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah.
Christopher A ReillyDepartment of Pharmacology and Toxicology, Center for Human Toxicology, University of Utah, Salt Lake City, Utah Chris.Reilly@pharm.utah.edu.
University of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI KATHARINE S ULLMAN · 1986 to 2026
$72.6M
TRP Channels and Air PollutionR01ES017431 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2009 to 2024
$5.3M
Pharmacogenomic and Metabolic Optimization of Glucocorticoid Therapy for AsthmaR01GM121648 · NIGMS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2017 to 2020
$2.5M
Pulmonary Epithelial TRPV3 and Wood Smoke InjuryR01ES027015 · NIEHS · UNIVERSITY OF UTAH · PI REILLY, CHRISTOPHER A · 2017 to 2021
$1.7M
NCRR Confocal ProposalS10RR024761 · NCRR · UNIVERSITY OF UTAH · PI RODESCH, CHRISTOPHER K · 2008 to 2008
$475k
NCI NIH HHS P30 CA042014NCRR NIH HHS S10 RR024761NIEHS NIH HHS R01 ES017431NIEHS NIH HHS R01 ES027015NIGMS NIH HHS R01 GM121648
6 · The paper itself

Abstract

This study investigated the roles of transient receptor potential (TRP) ankyrin-1 (TRPA1) and TRP vanilloid-3 (TRPV3) in regulating endoplasmic reticulum stress (ERS) and cytotoxicity in human bronchial epithelial cells (HBECs) treated with pneumotoxic wood smoke particulate matter (WSPM) and chemical agonists of each channel. Functions of TRPA1 and TRPV3 in pulmonary epithelial cells remain largely undefined. This study shows that TRPA1 activity localizes to the plasma membrane and endoplasmic reticulum (ER) of cells, whereas TRPV3 resides primarily in the ER. Additionally, treatment of cells using moderately cytotoxic concentrations of pine WSPM, carvacrol, and other TRPA1 agonists caused ERS as a function of both TRPA1 and TRPV3 activities. Specifically, ERS and cytotoxicity were attenuated by TRPA1 inhibition, whereas inhibiting TRPV3 exacerbated ERS and cytotoxicity. Interestingly, after treatment with pine WSPM, TRPA1 transcription was suppressed, whereas TRPV3 was increased. TRPV3 overexpression in HBECs conferred resistance to ERS and an attenuation of ERS-associated cell cycle arrest caused by WSPM and multiple prototypical ERS-inducing agents. Alternatively, short hairpin RNA-mediated knockdown of TRPV3, like the TRPV3 antagonist, exacerbated ERS. This study reveals previously undocumented roles for TRPA1 in promoting pathologic ERS and cytotoxicity elicited by pneumotoxic WSPM and TRPA1 agonists, and a unique role for TRPV3 in fettering pathologic facets of the integrated ERS response. SIGNIFICANCE STATEMENT: These findings provide new insights into how wood smoke particulate matter and other transient receptor potential ankyrin-1 (TRPA1) and transient receptor potential vanilloid-3 (TRPV3) agonists can affect human bronchial epithelial cells and highlight novel physiological and pathophysiological roles for TRPA1 and TRPV3 in these cells.

Indexed as

Cell LineCymenesEndoplasmic ReticulumEndoplasmic Reticulum StressEpithelial CellsHEK293 CellsHumansLungParticulate MatterPinusSmokeTransient Receptor Potential ChannelsTRPA1 Cation ChannelTRPV Cation ChannelsWoodcarvacrolCymenesParticulate MatterSmokeTransient Receptor Potential ChannelsTRPA1 Cation ChannelTRPA1 protein, humanTRPV3 protein, humanTRPV Cation Channels

Identifiers

PMID32938721
PMCPMC7569310
OpenAlexW3087711272

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.