Transient Receptor Potential Vanilloid-1 (TRPV1) Is a Mediator of Lung Toxicity for Coal Fly Ash Particulate Material

被引:51
作者
Deering-Rice, Cassandra E. [1 ]
Johansen, Mark E. [1 ]
Roberts, Jessica K. [1 ]
Thomas, Karen C. [1 ]
Romero, Erin G. [1 ]
Lee, Jeewoo [2 ]
Yost, Garold S. [1 ]
Veranth, John M. [1 ]
Reilly, Christopher A. [1 ]
机构
[1] Univ Utah, Dept Pharmacol & Toxicol, Salt Lake City, UT 84112 USA
[2] Seoul Natl Univ, Coll Pharm, Seoul, South Korea
基金
美国国家卫生研究院; 新加坡国家研究基金会;
关键词
DIESEL EXHAUST PARTICLES; CAPSAICIN RECEPTOR; CELL-DEATH; INFLAMMATORY CYTOKINES; PULMONARY INFLAMMATION; EPITHELIAL-CELLS; AIR-POLLUTION; ACTIVATION; EXPRESSION; TRPA1;
D O I
10.1124/mol.111.076067
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 4 alpha (C4 alpha), 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.
引用
收藏
页码:411 / 419
页数:9
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