Effect of fine particulate matter (PM2.5) collected in Hong Kong on mitochondrial permeability transition pore in human airway epithelial cells

Abstract

Background: Air pollution has been considered as the most significant environmental risk factor to human health. Fine particulate matter with aerodynamic diameter <2.5 µm (PM2.5) can penetrate into the lung reaching the large and small airways and even alveoli, causing adverse effect on the respiratory system. Our previous findings demonstrated the mitochondrial toxicity induced by PM2.5 exposure in airway cells. Recently, strong evidence is emerging that mitochondrial permeability transition pore (mPTP) may be important in certain physiological conditions and in the processes of cell damage and death. Thus, we aimed to study the effect of PM2.5 on mPTP in BEAS-2B cells. Methods: Atmospheric PM2.5 samples were collected by 47-mm Teflon filters using Desert Research Institute portable mid-volume samplers in the road site of Hong Kong. Human bronchial epithelial cell line BEAS-2B cells were cultured until 80% confluent. After arrest, cells were treated with different concentrations of PM2.5 samples to examine the ultracellular structure, intracellular calcium content, protein expressions of mPTP and apoptosis. Results: PM2.5 exposure caused mitochondrial swelling and structural damage on cristae from TEM images. In parallel, PM2.5 treatment significantly increased intracellular calcium content in a dose-dependent manner, which was accompanied by the upregulation of the major mPTP component voltage-dependent calcium channel (VDAC) expression as well as cell apoptosis. Conclusion: The current data suggest that exposure to PM2.5 collected in Hong Kong may cause mitochondriamediated apoptosis via promoting mPTP opening.