TY - JOUR
T1 - Exposing imidacloprid interferes with neurogenesis through impacting on chick neural tube cell survival
AU - Liu, Meng
AU - Wang, Guang
AU - Zhang, Shi-Yao
AU - Zhong, Shan
AU - Qi, Guo-Long
AU - Wang, Chao-Jie
AU - Chuai, Manli
AU - Lee, Kenneth Ka Ho
AU - Lu, Da-Xiang
AU - Yang, Xuesong
N1 - This study was supported by an NSFC grant (31401230, 81571436), Guangdong Natural Science Foundation (2016A030311044), the Science and Technology Planning Project of Guangdong Province (2014A020221091, 2014A020213008), the Science and Technology Program of Guangzhou (201510010073) and the Fundamental Research Funds for the Central Universities (21615421).
PY - 2016/7/21
Y1 - 2016/7/21
N2 - As a neonicotinoid pesticide, imidacloprid is widely used to control insects in agriculture and fleas on domestic animals. However, it is not known whether imidacloprid exposure negatively affects neurogenesis during embryonic development. In this study, using a chick embryo model, we investigated the effects of imidacloprid exposure on neurogenesis at the earliest stage and during late-stage embryo development. Exposing HH0 chick embryos to imidacloprid in EC culture caused neural tube defects (NTDs) and neuronal differentiation dysplasia as determined by NF/Tuj1 labeling. Furthermore, we found that F-actin accumulation on the apical side of the neural tube was suppressed by exposure to imidacloprid, and the expression of BMP4 and Shh on the dorsal and ventral sides of the neural tubes, respectively, were also reduced, which in turn affects the dorsolateral hinge points during bending of the neural plate. In addition, exposure to imidacloprid reduced cell proliferation and increased cell apoptosis, as determined by pHIS3 labeling and TUNEL staining, respectively, also contributing to the malformation. We obtained similar results in late-stage embryos exposed to imidacloprid. Finally, a bioinformatics analysis was employed to determine which genes identified in this study were involved in NTDs. The experimental evidence and bioinformatics analysis suggested that imidacloprid exposure during chick embryo development could increase the risk of NTDs and neural dysplasia.
AB - As a neonicotinoid pesticide, imidacloprid is widely used to control insects in agriculture and fleas on domestic animals. However, it is not known whether imidacloprid exposure negatively affects neurogenesis during embryonic development. In this study, using a chick embryo model, we investigated the effects of imidacloprid exposure on neurogenesis at the earliest stage and during late-stage embryo development. Exposing HH0 chick embryos to imidacloprid in EC culture caused neural tube defects (NTDs) and neuronal differentiation dysplasia as determined by NF/Tuj1 labeling. Furthermore, we found that F-actin accumulation on the apical side of the neural tube was suppressed by exposure to imidacloprid, and the expression of BMP4 and Shh on the dorsal and ventral sides of the neural tubes, respectively, were also reduced, which in turn affects the dorsolateral hinge points during bending of the neural plate. In addition, exposure to imidacloprid reduced cell proliferation and increased cell apoptosis, as determined by pHIS3 labeling and TUNEL staining, respectively, also contributing to the malformation. We obtained similar results in late-stage embryos exposed to imidacloprid. Finally, a bioinformatics analysis was employed to determine which genes identified in this study were involved in NTDs. The experimental evidence and bioinformatics analysis suggested that imidacloprid exposure during chick embryo development could increase the risk of NTDs and neural dysplasia.
KW - imidacloprid
KW - neural tube defect
KW - neuronal differentiation
KW - cell proliferation/apoptosis
KW - EMP4/Shh
U2 - 10.1093/toxsci/kfw111
DO - 10.1093/toxsci/kfw111
M3 - Article
C2 - 27444676
SN - 1096-6080
VL - 153
SP - 137
EP - 148
JO - Toxicological Sciences
JF - Toxicological Sciences
IS - 1
ER -