Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2015 (2015), Article ID 630361, 9 pages
Research Article

Modulation of Extracellular ATP Content of Mast Cells and DRG Neurons by Irradiation: Studies on Underlying Mechanism of Low-Level-Laser Therapy

1Acupuncture and Moxibustion College, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China
2Shanghai Research Center for Acupuncture and Meridians, 199 Guoshoujing Road, Shanghai 201203, China
3Research Centre, Centre Hospitalier de l’Université de Montréal (CRCHUM), Tour Viger, 900 rue Saint-Denis, Montréal, QC, Canada H2X 0A9
4Department of Medicine, Université de Montréal, CP 6128 Succursale Centre-Ville, Montréal, QC, Canada H3C 3T5
5Institute for Biophysics, Goethe-University Frankfurt, Max von Laue Straße 1, 60438 Frankfurt am Main, Germany

Received 11 May 2014; Revised 10 October 2014; Accepted 18 October 2014

Academic Editor: Jesús Pintor

Copyright © 2015 Lina Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Low-level-laser therapy (LLLT) is an effective complementary treatment, especially for anti-inflammation and wound healing in which dermis or mucus mast cells (MCs) are involved. In periphery, MCs crosstalk with neurons via purinergic signals and participate in various physiological and pathophysiological processes. Whether extracellular ATP, an important purine in purinergic signaling, of MCs and neurons could be modulated by irradiation remains unknown. In this study, effects of red-laser irradiation on extracellular ATP content of MCs and dorsal root ganglia (DRG) neurons were investigated and underlying mechanisms were explored in vitro. Our results show that irradiation led to elevation of extracellular ATP level in the human mast cell line HMC-1 in a dose-dependent manner, which was accompanied by elevation of intracellular ATP content, an indicator for ATP synthesis, together with [Ca2+]i elevation, a trigger signal for exocytotic ATP release. In contrast to MCs, irradiation attenuated the extracellular ATP content of neurons, which could be abolished by ARL 67156, a nonspecific ecto-ATPases inhibitor. Our results suggest that irradiation potentiates extracellular ATP of MCs by promoting ATP synthesis and release and attenuates extracellular ATP of neurons by upregulating ecto-ATPase activity. The opposite responses of these two cell types indicate complex mechanisms underlying LLLT.