Activation of TRPV1-dependent calcium oscillation exacerbates seawater inhalation-induced acute lung injury

Li,Congcong; Bo,Liyan; Liu,Qingqing; Liu,Wei; Chen,Xiangjun; Xu,Dunquan; Jin,Faguang

doi:10.3892/mmr.2016.4804

Activation of TRPV1-dependent calcium oscillation exacerbates seawater inhalation-induced acute lung injury

Authors:
- Congcong Li
- Liyan Bo
- Qingqing Liu
- Wei Liu
- Xiangjun Chen
- Dunquan Xu
- Faguang Jin
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Affiliations: Department of Respiration, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China, Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China
Published online on: January 20, 2016 https://doi.org/10.3892/mmr.2016.4804
Pages: 1989-1998
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Calcium is an important second messenger and it is widely recognized that acute lung injury (ALI) is often caused by oscillations of cytosolic free Ca2+. Previous studies have indicated that the activation of transient receptor potential‑vanilloid (TRPV) channels and subsequent Ca2+ entry initiates an acute calcium‑dependent permeability increase during ALI. However, whether seawater exposure induces such an effect through the activation of TRPV channels remains unknown. In the current study, the effect of calcium, a component of seawater, on the inflammatory reactions that occur during seawater drowning‑induced ALI, was examined. The results demonstrated that a high concentration of calcium ions in seawater increased lung tissue myeloperoxidase activity and the secretion of inflammatory mediators, such as tumor necrosis factor‑α (TNF‑α) and interleukin (IL)‑1β and IL‑6. Further study demonstrated that the seawater challenge elevated cytosolic Ca2+ concentration, indicated by [Ca2+]c, by inducing calcium influx from the extracellular medium via TRPV1 channels. The elevated [Ca2+c] may have resulted in the increased release of TNF‑α and IL‑1β via increased phosphorylation of nuclear factor‑κB (NF‑κB). It was concluded that a high concentration of calcium in seawater exacerbated lung injury, and TRPV1 channels were notable mediators of the calcium increase initiated by the seawater challenge. Calcium influx through TRPV1 may have led to greater phosphorylation of NF‑κB and increased release of TNF‑α and IL‑1β.

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