Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice
Parkinson’s disease (PD) is a common neurodegenerative movement disorder with undetermined etiology. A major pathological hallmark of PD is the progressive degeneration of dopaminergic neurons in the substantia nigra. Loss-of-function mutations in the RAB39B gene, which encodes a neuronal-specific s...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-01-01
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| Series: | Frontiers in Aging Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnagi.2023.1087823/full |
| _version_ | 1828054966611214336 |
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| author | Zijie Wang Zijie Wang Dingting Yang Dingting Yang Yiru Jiang Yong Wang Mengxi Niu Chong Wang Hong Luo Huaxi Xu Jingwen Li Yun-wu Zhang Xian Zhang |
| author_facet | Zijie Wang Zijie Wang Dingting Yang Dingting Yang Yiru Jiang Yong Wang Mengxi Niu Chong Wang Hong Luo Huaxi Xu Jingwen Li Yun-wu Zhang Xian Zhang |
| author_sort | Zijie Wang |
| collection | DOAJ |
| description | Parkinson’s disease (PD) is a common neurodegenerative movement disorder with undetermined etiology. A major pathological hallmark of PD is the progressive degeneration of dopaminergic neurons in the substantia nigra. Loss-of-function mutations in the RAB39B gene, which encodes a neuronal-specific small GTPase RAB39B, have been associated with X-linked intellectual disability and pathologically confirmed early-onset PD in multiple families. However, the role of RAB39B in PD pathogenesis remains elusive. In this study, we treated Rab39b knock-out (KO) mice with MPTP to explore whether RAB39B deficiency could alter MPTP-induced behavioral impairments and dopaminergic neuron degeneration. Surprisingly, we found that MPTP treatment impaired motor activity and led to loss of tyrosine hydroxylase-positive dopaminergic neurons and gliosis in both WT and Rab39b KO mice. However, RAB39B deficiency did not alter MPTP-induced impairments. These results suggest that RAB39B deficiency does not contribute to PD-like phenotypes through compromising dopaminergic neurons in mice; and its role in PD requires further scrutiny. |
| first_indexed | 2024-04-10T20:31:08Z |
| format | Article |
| id | doaj.art-c663de05c40c47fa9c79f597a65ca361 |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-04-10T20:31:08Z |
| publishDate | 2023-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-c663de05c40c47fa9c79f597a65ca3612023-01-25T06:35:23ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652023-01-011510.3389/fnagi.2023.10878231087823Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in miceZijie Wang0Zijie Wang1Dingting Yang2Dingting Yang3Yiru Jiang4Yong Wang5Mengxi Niu6Chong Wang7Hong Luo8Huaxi Xu9Jingwen Li10Yun-wu Zhang11Xian Zhang12Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaDepartment of Neurosurgery, Xiang’an Hospital of Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaDepartment of Neurosurgery, Xiang’an Hospital of Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaDepartment of Basic Medical Sciences, School of Medicine, Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaDepartment of Neurosurgery, Xiang’an Hospital of Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Medicine, Center for Brain Sciences, The First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Xiamen University, Xiamen, ChinaParkinson’s disease (PD) is a common neurodegenerative movement disorder with undetermined etiology. A major pathological hallmark of PD is the progressive degeneration of dopaminergic neurons in the substantia nigra. Loss-of-function mutations in the RAB39B gene, which encodes a neuronal-specific small GTPase RAB39B, have been associated with X-linked intellectual disability and pathologically confirmed early-onset PD in multiple families. However, the role of RAB39B in PD pathogenesis remains elusive. In this study, we treated Rab39b knock-out (KO) mice with MPTP to explore whether RAB39B deficiency could alter MPTP-induced behavioral impairments and dopaminergic neuron degeneration. Surprisingly, we found that MPTP treatment impaired motor activity and led to loss of tyrosine hydroxylase-positive dopaminergic neurons and gliosis in both WT and Rab39b KO mice. However, RAB39B deficiency did not alter MPTP-induced impairments. These results suggest that RAB39B deficiency does not contribute to PD-like phenotypes through compromising dopaminergic neurons in mice; and its role in PD requires further scrutiny.https://www.frontiersin.org/articles/10.3389/fnagi.2023.1087823/fullMPTPRAB39BPakinson’s diseasemouse behaviordopaminergic neurons |
| spellingShingle | Zijie Wang Zijie Wang Dingting Yang Dingting Yang Yiru Jiang Yong Wang Mengxi Niu Chong Wang Hong Luo Huaxi Xu Jingwen Li Yun-wu Zhang Xian Zhang Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice Frontiers in Aging Neuroscience MPTP RAB39B Pakinson’s disease mouse behavior dopaminergic neurons |
| title | Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice |
| title_full | Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice |
| title_fullStr | Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice |
| title_full_unstemmed | Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice |
| title_short | Loss of RAB39B does not alter MPTP-induced Parkinson’s disease-like phenotypes in mice |
| title_sort | loss of rab39b does not alter mptp induced parkinson s disease like phenotypes in mice |
| topic | MPTP RAB39B Pakinson’s disease mouse behavior dopaminergic neurons |
| url | https://www.frontiersin.org/articles/10.3389/fnagi.2023.1087823/full |
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