Biomedicine & Pharmacotherapy (Feb 2024)
miR-214-3p promotes the pathogenesis of Parkinson's disease by inhibiting autophagy
- Hui Dong,
- Jiahui Yan,
- Ping Huang,
- Xinyu Wang,
- Ru Zhang,
- Caiyun Zhang,
- Wenhui Wang,
- Wenxian Qian,
- Jin Zhou,
- Yunli Zhao,
- Jinghan Gao,
- Mengmeng Zhang,
- Xiuchang Ma,
- Zhizhong Wang,
- Changhua Yi,
- Jie Zhang,
- Wei Chen
Affiliations
- Hui Dong
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China
- Jiahui Yan
- Molecular Diagnostic Center, The Sixth Affiliated Hospital of Guangzhou Medical University/Qingyuan People's Hospital, Qingyuan 511518, China
- Ping Huang
- Department of Hepatology, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China
- Xinyu Wang
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China
- Ru Zhang
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China
- Caiyun Zhang
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Wenhui Wang
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Wenxian Qian
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Jin Zhou
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Yunli Zhao
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Jinghan Gao
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Mengmeng Zhang
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Xiuchang Ma
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China
- Zhizhong Wang
- Henan Key Laboratory of Brain Science and Brain-Computer Interface Technology, School of Electrical and Information Engineering, Zhengzhou University, Zhengzhou 450001, China
- Changhua Yi
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China; Corresponding authors at: Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
- Jie Zhang
- Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, 70 President Street, DDB410, Charleston, SC 29425, USA; Corresponding author.
- Wei Chen
- Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China; Corresponding authors at: Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
- Journal volume & issue
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Vol. 171
p. 116123
Abstract
Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by dopaminergic neuron death in the substantia nigra, leading to motor dysfunction. Autophagy dysregulation has been implicated in PD pathogenesis. This study explores the role of miR-214–3p in PD, focusing on its impact on autophagy and dopaminergic neuron viability. Using in vitro and in vivo models, we demonstrate that miR-214–3p inhibits autophagy and promotes dopaminergic neuron apoptosis. Behavioral assessments and molecular analyses reveal exacerbation of PD symptoms upon miR-214–3p overexpression. Furthermore, mechanistic investigations identify ATG3 as a target, shedding light on miR-214–3p's regulatory role in autophagy. These findings enhance our understanding of PD pathogenesis and propose miR-214–3p as a potential biomarker and therapeutic target for modulating autophagy and neuronal survival in PD.
