MiR-130 targetssynaptosomal-associated protein 25,which is involved in lead-induced presynaptic vesicle release and attention deficit disorder
作者单位：Department of Occupational ＆ Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment School of Public HealthFourth Military Medical University Department of Nutrition ＆ Food Hygiene and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment School of Public Health Fourth Military Medical University Precision Pharmacy ＆Drug Development Center Department of Pharmacy Tangdu Hospital Fourth Military Medical University
会议名称：《中国毒理学会第九次全国毒理学大会》
会议日期：2019年
学科分类：100405[医学-卫生毒理学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 10[医学]
摘 要：Lead（Pb） exposure causes long-term impairment in presynaptic transmitter release in the central nervous ***, the precise underlying mechanisms are unclear. MicroRNAs（miRNAs） regulating gene expression is a vital process for neuronal function. Through miR NA screening,we found that miR-130 was highly expressed in the anterior cingulate cortex（ACC） and hippocampus upon Pb exposure in mice. The dual luciferase assay demonstrated that miR-130 targeted synaptosomalassociated protein 25（SNAP-25） mRNA at nucleotides 555-561. Blocking miR-130 function in vitroor in vivoreversed the Pb-induced decrease in expression of its presynaptic target SNAP-25, leading tothe recovery of presynaptic vesicle release after Pb exposure, as well as the partial recovery of attention deficits in mice. Our study identified a critical target that miR-130 regulate SNAP-25 expression responsible for Pb caused presynaptic function impairment in ACC and mouse attentiondeficit disorder.
