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Critical Care: Critical Care Nonpulmonary |

Enhanced Production of Nitric Oxide in A549 Cells Through Activation of TRPA1 Ion Channel by Cold Stress FREE TO VIEW

Wenwu Sun, PhD; Zhonghua Wang, PhD; Zhuang Ma, MD; Haiyang Cui, PhD
Author and Funding Information

The General Hospital of Shenyang Military Region, Shenyang, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A172. doi:10.1016/j.chest.2016.02.178
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SESSION TITLE: Critical Care Nonpulmonary

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: 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). In the present study, we investigated the effect of cold stress on the change of NO. Furthermore, we tried to explore the underlying mechanism of the change of NO using NO and Ca2+ signaling fluorescence imaging.

METHODS: We measured the change of NO in single cell with DACF-DA and the change in cytosolic Ca2+ concentration ([Ca2+]c) in A549 cell.

RESULTS: We observed that cold stress (from 20℃ to 5℃) induced an increase of NO in A549 cell, which was completely abolished by applying an extracellular Ca2+ 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 [Ca2+]c in A549 cell. Additionally, TRPA1 inhibitor, Ruthenium red (RR) and camphor, significantly blocked the enhanced production of NO and the rise of [Ca2+]c induced by AITC or cold stimulation, respectively.

CONCLUSIONS: Taken together, theses data indicated that cold-induced TRPA1 activation was responsible for the enhanced production of NO in A549 cell.

CLINICAL IMPLICATIONS: This work demonstrated a mechanism of cold-induced the enhanced production of NO in lung epithelial cell, which might augment the understanding of physiology, pathology and treatment in the pulmonary system.

DISCLOSURE: The following authors have nothing to disclose: Wenwu Sun, Zhonghua Wang, Zhuang Ma, Haiyang Cui

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