MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells
Parkinson’s disease (PD) is a neurodegenerative disorder causing severe social and economic burdens. The origin of PD has been usually attributed to mitochondrial dysfunction. To this end, mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis. Previously...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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China Science Publishing & Media Ltd.
2022-07-01
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| Series: | Acta Biochimica et Biophysica Sinica |
| Subjects: | |
| Online Access: | https://www.sciengine.com/doi/10.3724/abbs.2022098 |
| _version_ | 1797635380935131136 |
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| author | Zhu Shun Xu Nan Han Yanyan Ye Xiaofei Yang Ling Zuo Ji Liu Wen |
| author_facet | Zhu Shun Xu Nan Han Yanyan Ye Xiaofei Yang Ling Zuo Ji Liu Wen |
| author_sort | Zhu Shun |
| collection | DOAJ |
| description | Parkinson’s disease (PD) is a neurodegenerative disorder causing severe social and economic burdens. The origin of PD has been usually attributed to mitochondrial dysfunction. To this end, mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis. Previously, we found that the expression of mitochondrial transcription termination factor 3 (MTERF3) was reduced in MPP+-induced mice model of PD. In the present study, we probe the function of MTERF3 and its role in MPP+-induced cellular model of PD. Initially, we observe that MTERF3 expression is also reduced in MPP+-induced cellular model of PD, which can be mainly attributed to the increase of MTERF3 degradation. Next, we examine the effect of MTERF3 knockdown and overexpression on the replication, transcription, and translation of mitochondrial DNA (mtDNA). We show that knockdown and overexpression of MTERF3 have opposite effects on mtDNA transcript level but similar effects on mtDNA expression level, in line with MTERF3’s dual roles in mtDNA transcription and translation. In addition, we examine the effect of MTERF3 knockdown and overexpression on mitochondrial function with and without MPP+ treatment, and find that MTERF3 seems to play a generally protective role in MPP+-induced mitochondrial dysfunction. Together, this work suggests a regulatory role of MTERF3 in MPP+-induced cellular model of PD and may provide clues in designing novel therapeutics against PD. |
| first_indexed | 2024-03-11T12:21:15Z |
| format | Article |
| id | doaj.art-e7cac81a7ba64d63948b070365d97749 |
| institution | Directory Open Access Journal |
| issn | 1672-9145 |
| language | English |
| last_indexed | 2024-03-11T12:21:15Z |
| publishDate | 2022-07-01 |
| publisher | China Science Publishing & Media Ltd. |
| record_format | Article |
| series | Acta Biochimica et Biophysica Sinica |
| spelling | doaj.art-e7cac81a7ba64d63948b070365d977492023-11-07T01:01:03ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452022-07-01541113112110.3724/abbs.202209820d259ccMTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cellsZhu Shun0Xu Nan1Han Yanyan2Ye Xiaofei3Yang Ling4Zuo Ji5Liu Wen6[][][][][][][]Parkinson’s disease (PD) is a neurodegenerative disorder causing severe social and economic burdens. The origin of PD has been usually attributed to mitochondrial dysfunction. To this end, mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis. Previously, we found that the expression of mitochondrial transcription termination factor 3 (MTERF3) was reduced in MPP+-induced mice model of PD. In the present study, we probe the function of MTERF3 and its role in MPP+-induced cellular model of PD. Initially, we observe that MTERF3 expression is also reduced in MPP+-induced cellular model of PD, which can be mainly attributed to the increase of MTERF3 degradation. Next, we examine the effect of MTERF3 knockdown and overexpression on the replication, transcription, and translation of mitochondrial DNA (mtDNA). We show that knockdown and overexpression of MTERF3 have opposite effects on mtDNA transcript level but similar effects on mtDNA expression level, in line with MTERF3’s dual roles in mtDNA transcription and translation. In addition, we examine the effect of MTERF3 knockdown and overexpression on mitochondrial function with and without MPP+ treatment, and find that MTERF3 seems to play a generally protective role in MPP+-induced mitochondrial dysfunction. Together, this work suggests a regulatory role of MTERF3 in MPP+-induced cellular model of PD and may provide clues in designing novel therapeutics against PD.https://www.sciengine.com/doi/10.3724/abbs.2022098MTERF3mitochondrial dysfunctiondegenerative diseaseenvironmental toxinsParkinson’s disease |
| spellingShingle | Zhu Shun Xu Nan Han Yanyan Ye Xiaofei Yang Ling Zuo Ji Liu Wen MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells Acta Biochimica et Biophysica Sinica MTERF3 mitochondrial dysfunction degenerative disease environmental toxins Parkinson’s disease |
| title | MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells |
| title_full | MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells |
| title_fullStr | MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells |
| title_full_unstemmed | MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells |
| title_short | MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells |
| title_sort | mterf3 contributes to mpp induced mitochondrial dysfunction in sh sy5y cells |
| topic | MTERF3 mitochondrial dysfunction degenerative disease environmental toxins Parkinson’s disease |
| url | https://www.sciengine.com/doi/10.3724/abbs.2022098 |
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