title: Enhanced production of nitric oxide in A549 cells through activation of TRPA1 ion channel by cold stress.
abstract: The respiratory epithelium is exposed to the external environment, and inhalation of cold air is common during the season of winter. In addition, the lung is a major source of nitric oxide (NO). However, the effect of cold stress on the production of NO is still unclear. In the present work, We measured the change of NO in single cell with DACF-DA and the change in cytosolic Ca(2+) concentration ([Ca(2+)]c) in A549 cell. We observed that cold stress (from 20 °C to 5 °C) induced an increase of NO in A549 cell, which was completely abolished by applying an extracellular Ca(2+) free medium. Further experiments showed that cold-sensing transient receptor potential subfamily member 1 (TRPA1) channel agonist (allyl isothiocyanate, AITC) increased the production of NO and the level of [Ca(2+)]c in A549 cell. Additionally, TRPA1 inhibitor, Ruthenium red (RR) and camphor, significantly blocked the enhanced production of NO and the rise of [Ca(2+)]c induced by AITC or cold stimulation, respectively. Taken together, these data indicated that cold-induced TRPA1 activation was responsible for the enhanced production of NO in A549 cell.
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, 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, 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, Shenyang 110840, China.
authors.forename: Jianping
authors.initials: J
authors.lastname: Cao
authors.affiliation: Department of Experimental Medicine, Northern Hospital, Shenyang 110840, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Institute of Cardiovascular Research of People's Liberation Army, Shenyang Northern Hospital, Shenyang 110840, China. Electronic address: hanyalin53@gmail.com.
authors.forename: Yaling
authors.initials: Y
authors.lastname: Han
authors.affiliation: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, Shenyang 110840, China. Electronic address: mzm0404@yahoo.com.
authors.forename: Zhuang
authors.initials: Z
authors.lastname: Ma
mesh_terms: D015220:Calcium Channels / Q000378:metabolism*; D002164:Camphor / Q000494:pharmacology; D003080:Cold Temperature; D058639:Cold-Shock Response; D006801:Humans; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D012430:Ruthenium Red / Q000494:pharmacology; D000074025:TRPA1 Cation Channel; D050051:Transient Receptor Potential Channels / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D015220:Calcium Channels; D009419:Nerve Tissue Proteins; D000074025:TRPA1 Cation Channel; C473350:TRPA1 protein, human; D050051:Transient Receptor Potential Channels; D012430:Ruthenium Red; D009569:Nitric Oxide; D002164:Camphor
keywords: Cold stress; Nitric oxide; TRPA1; [Ca(2+)](c)