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Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material.
Chem Res Toxicol. 2013 May 20; 26(5):750-8.CR

Abstract

Cigarette smoke, diesel exhaust, and other combustion-derived particles activate the calcium channel transient receptor potential ankyrin-1 (TRPA1), causing irritation and inflammation in the respiratory tract. It was hypothesized that wood smoke particulate and select chemical constituents thereof would also activate TRPA1 in lung cells, potentially explaining the adverse effects of wood and other forms of biomass smoke on the respiratory system. TRPA1 activation was assessed using calcium imaging assays in TRPA1-overexpressing HEK-293 cells, mouse primary trigeminal neurons, and human adenocarcinoma (A549) lung cells. Particles from pine and mesquite smoke were less potent agonists of TRPA1 than an equivalent mass concentration of an ethanol extract of diesel exhaust particles; pine particles were comparable in potency to cigarette smoke condensate, and mesquite particles were the least potent. The fine particulate (PM < 2.5 μm) of wood smoke were the most potent TRPA1 agonists and several chemical constituents of wood smoke particulate, 3,5-ditert-butylphenol, coniferaldehyde, formaldehyde, perinaphthenone, agathic acid, and isocupressic acid, were TRPA1 agonists. Pine particulate activated TRPA1 in mouse trigeminal neurons and A549 cells in a concentration-dependent manner, which was inhibited by the TRPA1 antagonist HC-030031. TRPA1 activation by wood smoke particles occurred through the electrophile/oxidant-sensing domain (i.e., C621/C641/C665/K710), based on the inhibition of cellular responses when the particles were pretreated with glutathione; a role for the menthol-binding site of TRPA1 (S873/T874) was demonstrated for 3,5-ditert-butylphenol. This study demonstrated that TRPA1 is a molecular sensor for wood smoke particulate and several chemical constituents thereof, in sensory neurons and A549 cells, suggesting that TRPA1 may mediate some of the adverse effects of wood smoke in humans.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, University of Utah , 30 S. 2000 E., Room 201 Skaggs Hall, Salt Lake City, Utah 84112, United States.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23541125

Citation

Shapiro, Darien, et al. "Activation of Transient Receptor Potential Ankyrin-1 (TRPA1) in Lung Cells By Wood Smoke Particulate Material." Chemical Research in Toxicology, vol. 26, no. 5, 2013, pp. 750-8.
Shapiro D, Deering-Rice CE, Romero EG, et al. Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material. Chem Res Toxicol. 2013;26(5):750-8.
Shapiro, D., Deering-Rice, C. E., Romero, E. G., Hughen, R. W., Light, A. R., Veranth, J. M., & Reilly, C. A. (2013). Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material. Chemical Research in Toxicology, 26(5), 750-8. https://doi.org/10.1021/tx400024h
Shapiro D, et al. Activation of Transient Receptor Potential Ankyrin-1 (TRPA1) in Lung Cells By Wood Smoke Particulate Material. Chem Res Toxicol. 2013 May 20;26(5):750-8. PubMed PMID: 23541125.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material. AU - Shapiro,Darien, AU - Deering-Rice,Cassandra E, AU - Romero,Erin G, AU - Hughen,Ronald W, AU - Light,Alan R, AU - Veranth,John M, AU - Reilly,Christopher A, Y1 - 2013/04/25/ PY - 2013/4/2/entrez PY - 2013/4/2/pubmed PY - 2014/12/23/medline SP - 750 EP - 8 JF - Chemical research in toxicology JO - Chem Res Toxicol VL - 26 IS - 5 N2 - Cigarette smoke, diesel exhaust, and other combustion-derived particles activate the calcium channel transient receptor potential ankyrin-1 (TRPA1), causing irritation and inflammation in the respiratory tract. It was hypothesized that wood smoke particulate and select chemical constituents thereof would also activate TRPA1 in lung cells, potentially explaining the adverse effects of wood and other forms of biomass smoke on the respiratory system. TRPA1 activation was assessed using calcium imaging assays in TRPA1-overexpressing HEK-293 cells, mouse primary trigeminal neurons, and human adenocarcinoma (A549) lung cells. Particles from pine and mesquite smoke were less potent agonists of TRPA1 than an equivalent mass concentration of an ethanol extract of diesel exhaust particles; pine particles were comparable in potency to cigarette smoke condensate, and mesquite particles were the least potent. The fine particulate (PM < 2.5 μm) of wood smoke were the most potent TRPA1 agonists and several chemical constituents of wood smoke particulate, 3,5-ditert-butylphenol, coniferaldehyde, formaldehyde, perinaphthenone, agathic acid, and isocupressic acid, were TRPA1 agonists. Pine particulate activated TRPA1 in mouse trigeminal neurons and A549 cells in a concentration-dependent manner, which was inhibited by the TRPA1 antagonist HC-030031. TRPA1 activation by wood smoke particles occurred through the electrophile/oxidant-sensing domain (i.e., C621/C641/C665/K710), based on the inhibition of cellular responses when the particles were pretreated with glutathione; a role for the menthol-binding site of TRPA1 (S873/T874) was demonstrated for 3,5-ditert-butylphenol. This study demonstrated that TRPA1 is a molecular sensor for wood smoke particulate and several chemical constituents thereof, in sensory neurons and A549 cells, suggesting that TRPA1 may mediate some of the adverse effects of wood smoke in humans. SN - 1520-5010 UR - https://www.unboundmedicine.com/medline/citation/23541125/Activation_of_transient_receptor_potential_ankyrin_1__TRPA1__in_lung_cells_by_wood_smoke_particulate_material_ L2 - https://doi.org/10.1021/tx400024h DB - PRIME DP - Unbound Medicine ER -