Enhanced production of nitric oxide in A549 cells through activation of TRPA1 ion channel by cold stress.

Wenwu Sun, Zhonghua Wang, Jianping Cao, Xu Wang, Yaling Han, Zhuang Ma

Journal: Nitric oxide : biology and chemistry 2015;40():31-5

PMID: 24815021

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.

Copyright © 2014 Elsevier Inc. All rights reserved.

Address: Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, Shenyang 110840, China.; Department of Experimental Medicine, Northern Hospital, Shenyang 110840, China.; Department of Cardiology, Institute of Cardiovascular Research of People's Liberation Army, Shenyang Northern Hospital, Shenyang 110840, China. Electronic address: [email protected].; Department of Respiratory Medicine, General Hospital of Shenyang Military Area Command, Shenyang 110840, China. Electronic address: [email protected].
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