Zhang Jun-Li, Sun Wen-Wu, Cao Jian-Ping, Ma Zhuang*


Department of Pulmonary and Critical Care Medicine, General Hospital of Northern Theater Command, Shenyang City, Liaoning Province, 110016, China


Introducion: Acrolein is present in cigarette smoke, vehicle exhaust, and air pollution. It has been reported that acrolein activates nuclear factor-erythroid 2 related factor2 (Nrf2) signaling pathway in lung epithelial cells. Acrolein is also known as one of transient receptor potential ankyrin-repeat 1 channel (TRPA1) agonists. However, the role of TRPA1 in the Nrf2 nuclear translocation caused by acrolein remains elusive.

Material and methods: In the present work, the change of Nrf2 nuclear translocation was analyzed by immunocytochemistry. At the same time, cytosolic Ca2+ concentration ([Ca2+]c) was examined in A549 cells stimulated by acrolein.

Results: Results showed that Nrf2 nuclear translocation was enhanced by acrolein in A549 cells, which was abolished by AP-18 (a TRPA1 channel blocker). In addition, AP-18 blocked enhanced [Ca2+]c induced by acrolein. The further experiments confirmed that removal of extracellular Ca2+ largely abrogated the [Ca2+]c elevation and nuclear translocation of Nrf2 induced by acrolein simultaneously.

Conclusions: Our results suggest that acrolein induces Nrf2 nuclear translocation through activation of TRPA1 in lung epithelial cells, which might be useful in the research and treatment of pulmonary disease. 


Nrf2, Acrolein, TRPA1, [Ca2+]c.