Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material.
Activation of transient receptor potential ankyrin-1 (TRPA1) in lung cells by wood smoke particulate material.
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DOI：
10.1021/tx400024h
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发表时间：
2013-05-20
影响因子：
4.1
通讯作者：
Reilly CA
中科院分区：
文献类型：
--
作者：
Shapiro D;Deering-Rice CE;Romero EG;Hughen RW;Light AR;Veranth JM;Reilly CA
香烟烟雾、柴油废气和其他燃烧产生的颗粒激活钙通道瞬时受体电位锚蛋白-1 (TRPA1)，引起呼吸道刺激和炎症。据推测，木材烟雾颗粒及其特定化学成分也会激活肺细胞中的TRPA1，这可能解释了木材和其他形式的生物质烟雾对呼吸系统的不利影响。在TRPA1过表达的HEK-293细胞、小鼠原代三叉神经细胞和人腺癌（A549）肺细胞中，采用钙显像法评估TRPA1的激活情况。与同等质量浓度的柴油尾气颗粒的乙醇提取物相比，来自松树和豆科植物烟雾的颗粒对TRPA1的激动作用更弱；松木颗粒的效力与香烟烟雾凝结物相当，豆科植物颗粒的效力最低。木材烟雾的细颗粒物（PM<2.5 μm）是最有效的TRPA1激动剂，木材烟雾颗粒的化学成分：3,5-二叔丁基酚、松柏醛、甲醛、环萘醌、agathic酸和异柏酸是TRPA1激动剂。松木颗粒对小鼠三叉神经细胞和A549细胞中的TRPA1呈浓度依赖性激活，TRPA1拮抗剂HC-030031对其有抑制作用。木烟颗粒经谷胱甘肽预处理后可抑制细胞反应，通过亲电/氧化感应结构域（即C621/C641/C665/K710）激活TRPA1；TRPA1的薄荷醇结合位点（S873/T874）被证实对3,5-二叔丁基苯酚起作用。本研究表明，TRPA1在感觉神经元和A549细胞中是木材烟雾颗粒及其几种化学成分的分子传感器，提示TRPA1可能介导了人类木材烟雾的一些不良反应。
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 pre-treated 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.
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影响因子：
20.8
作者：
DOCKERY, DW;POPE, CA
通讯作者：
POPE, CA
影响因子：
10.4
作者：
Li J;Kanju P;Patterson M;Chew WL;Cho SH;Gilmour I;Oliver T;Yasuda R;Ghio A;Simon SA;Liedtke W
通讯作者：
Liedtke W
影响因子：
11.4
作者：
McDonald, JD;Zielinska, B;Watson, JG
通讯作者：
Watson, JG
影响因子：
7.4
作者：
Grosjean, E;Green, PG;Grosjean, D
通讯作者：
Grosjean, D
DOI：
10.1513/pats.201001-004sm
发表时间：
2010-07-01
期刊：
Proceedings of the American Thoracic Society
影响因子：
--
作者：
Bessac, Bret F;Jordt, Sven-Eric
通讯作者：
Jordt, Sven-Eric