TY - JOUR
T1 - Fine particulate matter induces endoplasmic reticulum stress-mediated apoptosis in human SH-SY5Y cells
AU - Zhang, Mei
AU - Wang , Ying
AU - Wong, Ricky M.S.
AU - Yung, Ken Kin Lam
AU - Li, Ruijin
N1 - Funding Information:
This work was supported by the National Natural Science Foundation of China ( 91843301 ), Nature Science Foundation of Shanxi Province in China ( 201801D121260 ), Project on Social Development by the Shanxi Science and Technology Department ( 201903D321079 ), Training Program of Outstanding Achievement of Higher Education Institutions in Shanxi ( 2019KJ003 ) and Hundred Talents Program of Shanxi Province in China .
Publisher Copyright:
© 2021 Elsevier B.V.
PY - 2022/1
Y1 - 2022/1
N2 - 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 μg/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 IER1α 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/Caspase12) 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.
AB - 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 μg/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 IER1α 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/Caspase12) 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.
KW - Apoptosis
KW - Endoplasmic reticulum stress
KW - Fine particulate matter
KW - Human SH-SY5Y cells
UR - http://www.scopus.com/inward/record.url?scp=85120061799&partnerID=8YFLogxK
U2 - 10.1016/j.neuro.2021.11.012
DO - 10.1016/j.neuro.2021.11.012
M3 - Journal article
AN - SCOPUS:85120061799
SN - 0161-813X
VL - 88
SP - 187
EP - 195
JO - NeuroToxicology
JF - NeuroToxicology
ER -
