Tiethof Angela K, Richardson Jason R, Hart Ronald P
Joint Program in Toxicology, Environmental and Occupational Health Science Institute, Rutgers University, Piscataway, NJ 08854, USA.
Environmental Health Sciences, Robert Stempel School of Public Health and Social Work, Florida International University, Miami, FL 33199, USA.
Toxics. 2018 Sep 1;6(3):52. doi: 10.3390/toxics6030052.
Butyrylcholinesterase (BChE) is the evolutionary counterpart to acetylcholinesterase (AChE). Both are expressed early in nervous system development prior to cholinergic synapse formation. The organophosphate pesticide chlorpyrifos (CPF) primarily exerts toxicity through the inhibition of AChE, which results in excess cholinergic stimulation at the synapse. We hypothesized that the inhibition of AChE and BChE by CPF may impair early neurogenesis in neural stem cells (NSCs). To model neurodevelopment in vitro, we used human NSCs derived from induced pluripotent stem cells (iPSCs) with a focus on the initial differentiation mechanisms. Over the six days of NSC differentiation, the BChE activity and mRNA expression significantly increased, while the AChE activity and expression remained unchanged. The CPF treatment (10 μM) caused 82% and 92% inhibition of AChE and BChE, respectively. The CPF exposure had no effect on the cell viability or the expression of the differentiation markers HES5, DCX, or MAP2. However, the shRNA-knockdown of the BChE expression resulted in the decreased or delayed expression of the transcription factors HES5 and HES3. BChE may have a role in the differentiation of NSCs independent of, or in addition to, its enzymatic activity.
丁酰胆碱酯酶(BChE)是乙酰胆碱酯酶(AChE)在进化上的对应物。两者都在胆碱能突触形成之前的神经系统发育早期表达。有机磷农药毒死蜱(CPF)主要通过抑制AChE发挥毒性作用,这会导致突触处胆碱能刺激过度。我们推测CPF对AChE和BChE的抑制可能会损害神经干细胞(NSC)的早期神经发生。为了在体外模拟神经发育,我们使用了源自诱导多能干细胞(iPSC)的人NSC,重点关注初始分化机制。在NSC分化的六天时间里,BChE活性和mRNA表达显著增加,而AChE活性和表达保持不变。CPF处理(10μM)分别导致AChE和BChE抑制82%和92%。CPF暴露对细胞活力或分化标志物HES5、DCX或MAP2的表达没有影响。然而,BChE表达的shRNA敲低导致转录因子HES5和HES3的表达降低或延迟。BChE可能在NSC的分化中发挥作用,这与其酶活性无关或除此之外还另有作用。