title: Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells.
abstract: Reactive oxygen species (ROS) are responsible for lung damage during inhalation of cold air. However, the mechanism of the ROS production induced by cold stress in the lung is still unclear. In this work, we measured the changes of ROS and the cytosolic Ca(2+) concentration ([Ca(2+)]c) in A549 cell. We observed that cold stress (from 20 to 5 °C) exposure of A549 cell resulted in an increase of ROS and [Ca(2+)]c, which was completely attenuated by removing Ca(2+) from medium. Further experiments showed that cold-sensing transient receptor potential subfamily member 1 (TRPA1) agonist (allyl isothiocyanate, AITC) increased the production of ROS and the level of [Ca(2+)]c in A549 cell. Moreover, HC-030031, a TRPA1 selective antagonist, significantly inhibited the enhanced ROS and [Ca(2+)]c induced by AITC or cold stimulation, respectively. Taken together, these data demonstrated that TRPA1 activation played an important role in the enhanced production of ROS induced by cold stress in A549 cell.
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, No. 83, Wenhua Road, Shenhe District, Shenyang, 110840, China.
authors.forename: Wenwu
authors.initials: W
authors.lastname: Sun
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, No. 83, Wenhua Road, Shenhe District, Shenyang, 110840, China.
authors.forename: Zhonghua
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, No. 83, Wenhua Road, Shenhe District, Shenyang, 110840, China.
authors.forename: Jianping
authors.initials: J
authors.lastname: Cao
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, No. 83, Wenhua Road, Shenhe District, Shenyang, 110840, China.
authors.forename: Haiyang
authors.initials: H
authors.lastname: Cui
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, No. 83, Wenhua Road, Shenhe District, Shenyang, 110840, China. ma-tianyi@163.com.
authors.forename: Zhuang
authors.initials: Z
authors.lastname: Ma
mesh_terms: D000072283:A549 Cells; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D003080:Cold Temperature; D058639:Cold-Shock Response; D006801:Humans; D009419:Nerve Tissue Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*; D000074025:TRPA1 Cation Channel; D050051:Transient Receptor Potential Channels / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D009419:Nerve Tissue Proteins; D017382:Reactive Oxygen Species; D000074025:TRPA1 Cation Channel; C473350:TRPA1 protein, human; D050051:Transient Receptor Potential Channels; D002118:Calcium
keywords: Cold stress; Reactive oxygen species; TRPA1; [Ca2+]c