Fine particulate matter induces endoplasmic reticulum stress-mediated apoptosis in human SH-SY5Y cells

Exposure to ambient fine particulate matter (PM2.5) may contribute to brain injury, however, the molecular mechanisms have not yet been fully described. In this study, the human SH-SY5Y cells were treated with PM2.5 with different concentrations (0, 25, 100, and 250 mu g/mL) for 24 h to investigate the cell apoptosis mediated by endoplasmic reticulum (ER) stress. The ratio of apoptosis, Ca2+ level, biomarkers of ER stress and apoptosis were determined. The results revealed that PM2.5 triggered the increase of apoptosis ratio and cellular Ca2+ levels. Compared with control, the expression of GRP78 and phosphorylation of IER1 alpha and p38 were enhanced significantly in the cells under the conditions of PM2.5 exposure for activating ER stress signals. Besides, the key genes (CHOP/DR5/Caspase8/Caspasel 2) in ER stress-induced apoptosis signals were up-regulated after the PM2.5 treatment compared to the control. The results suggested PM2.5 induced apoptosis in SH-SY5Y cells by the stimulation of ER stress, which may be the potential mechanism of neurological diseases incurred by PM2.5.

Automated summary

The study found that PM2.5 can induce apoptosis in SH-SY5Y cells by activating endoplasmic reticulum stress signals, which may be a potential mechanism of neurological diseases caused by PM2.5.