Particulate matter (PM2.5) exposure season-dependently induces neuronal apoptosis and synaptic injuries

Epidemiological studies have shown that particulate matter 2.5 (PM2.5) not only increases the incidence of cardiopulmonary illnesses but also relates to the development of neurodegenerative diseases. Considering that PM, 5 is highly heterogeneous with regional disparity and seasonal variation, we investigated whether PM, exposure induced neuronal apoptosis and synaptic injuries in a season-dependent manner. The results indicated that PM,., altered the expression of apoptosis-related proteins (mainly bax and bcl-2), activated caspase-3 and caused neuronal apoptosis. Additionally, PIV12., decreased the levels of synaptic structural protein postsynaptic density (PSD-95) and synaptic functional protein N-methyl-D-aspartate (NMDA) receptor subunit (NR2B) expression. These effects occurred in a season-dependent manner, and PM, collected from the winter showed the strongest changes. Furthermore, the effect was coupled with the inhibition of phosphorylated extra cellular signal-regulated kinase 1/2 (p-ERK1/2) and phosphorylated cAMP-response element binding protein (p-CREB). Based on the findings, we analyzed the correlations between the chemical composition of PM, 5 samples and the biological effects, and confirmed that winter PM, 5 played a major role in causing neuronal apoptosis and synaptic injuries among different season samples. (C) 2016 The Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences. Published by Elsevier B.V.