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Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

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Cell Stress and Chaperones Aims and scope

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 Ca2+ concentration ([Ca2+]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 [Ca2+]c, which was completely attenuated by removing Ca2+ 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 [Ca2+]c in A549 cell. Moreover, HC-030031, a TRPA1 selective antagonist, significantly inhibited the enhanced ROS and [Ca2+]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.

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Acknowledgments

This work was supported by the 12th 5 years project of medicine (No. BWS12J007), The Natural Sciences Foundation of Liaoning Province (No. 2011225008), and the National S&T project (No. 2012ZX09303-016).

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Correspondence to Zhuang Ma.

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Sun, W., Wang, Z., Cao, J. et al. Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells. Cell Stress and Chaperones 21, 367–372 (2016). https://doi.org/10.1007/s12192-015-0663-3

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  • DOI: https://doi.org/10.1007/s12192-015-0663-3

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