机构:[1]Central Laboratory and Department of Neurology, Shunde Hospital, Southern Medical University (The First People’s Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China[2]Key Laboratory of Mental Health of the Ministry of Education, Southern Medical University, Guangzhou, 510515, Guangdong, China[3]Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Foshan, 528000, Guangdong, China[4]Teaching Center of Experimental Medicine, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, Guangdong, China[5]Department of Encephalopathy, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China大德路总院脑病科广东省中医院[6]Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510030, Guangdong, China
Parkinson's disease (PD) features the degeneration and death of dopamine neurons in the substantia nigra pars compacta and the formation of Lewy bodies that contain alpha-synuclein. Among the numerous PD etiologies, glutamate excitotoxicity is a research hot spot, and glutamate transporters play key roles in this theory. It has been shown that the expression of the glutamate transporter is regulated by microRNAs. In this study, we found that the levels of expression and function of glutamate transporter type 1 (GLT-1) were significantly reduced and miR-543-3p was upregulated during the development of PD. Furthermore, our results indicated that GLT-1 plays an important role in the pathomechanism of PD. We found that miR-543-3p can suppress the expression and function of GLT-1 in MPP+-treated astrocytes and MPTP-treated mice. Inhibition of miR-543-3p can rescue the expression and function of GLT-1 and relieve dyskinesia in the PD model, which suggests that inhibition of miR-543-3p could serve as a potential therapeutic target for PD.
基金:
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81870991, U1603281, 31570716]; Science and Technology Planning Project of Guangdong Province [2012B050200003, 2013B021800305, 2016A050502025]; Science and Technology Planning Project of Guangzhou [2013J4500018, 2014J4100008]; Program for Changjiang Scholars and Innovative Research Team in UniversityProgram for Changjiang Scholars & Innovative Research Team in University (PCSIRT) [IRT_16R37]; Clinical Research startup program of Southern Medical University by High-level University Construction Funding of Guangdong Provincial Department of Education [LC2016PY055]
第一作者机构:[1]Central Laboratory and Department of Neurology, Shunde Hospital, Southern Medical University (The First People’s Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China[2]Key Laboratory of Mental Health of the Ministry of Education, Southern Medical University, Guangzhou, 510515, Guangdong, China
共同第一作者:
通讯作者:
通讯机构:[1]Central Laboratory and Department of Neurology, Shunde Hospital, Southern Medical University (The First People’s Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China[2]Key Laboratory of Mental Health of the Ministry of Education, Southern Medical University, Guangzhou, 510515, Guangdong, China[5]Department of Encephalopathy, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China[6]Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510030, Guangdong, China[*1]Central Laboratory and Department of Neurology, Shunde Hospital, Southern Medical University (The First People’s Hospital of Shunde Foshan), Foshan, 528300, Guangdong, China, and Key Laboratory of Mental Health of the Ministry of Education[*2]Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510030, Guangdong, China[*3]Department of Encephalopathy, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China
推荐引用方式(GB/T 7714):
Wu Xiaojuan,Meng Xingjun,Tan Feng,et al.Regulatory Mechanism of miR-543-3p on GLT-1 in a Mouse Model of Parkinson's Disease[J].ACS CHEMICAL NEUROSCIENCE.2019,10(3):1791-1800.doi:10.1021/acschemneuro.8b00683.
APA:
Wu, Xiaojuan,Meng, Xingjun,Tan, Feng,Jiao, Zhigang,Zhang, Xiupin...&Qu, Shaogang.(2019).Regulatory Mechanism of miR-543-3p on GLT-1 in a Mouse Model of Parkinson's Disease.ACS CHEMICAL NEUROSCIENCE,10,(3)
MLA:
Wu, Xiaojuan,et al."Regulatory Mechanism of miR-543-3p on GLT-1 in a Mouse Model of Parkinson's Disease".ACS CHEMICAL NEUROSCIENCE 10..3(2019):1791-1800