Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease
This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson’s disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differ...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Parkinson's Disease |
| Online Access: | http://dx.doi.org/10.1155/2021/9919129 |
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| _version_ | 1832563237696045056 |
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| author | Wei Quan Jia Li Li Liu Qinghui Zhang Yidan Qin Xiaochen Pei Jiajun Chen |
| author_facet | Wei Quan Jia Li Li Liu Qinghui Zhang Yidan Qin Xiaochen Pei Jiajun Chen |
| author_sort | Wei Quan |
| collection | DOAJ |
| description | This study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson’s disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differentially expressed genes and function enrichment analysis of the two sets of data and found that the expression of the m6A-modification gene HNRNPC was significantly downregulated in the PD group, and it played an important role in DNA metabolism, RNA metabolism, and RNA processing and may be involved in PD. Then, we constructed the HNRNPC differential expression cell line to study the role of this gene in the pathogenesis of PD. The results showed that overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors IFN-β, IL-6, and TNF-α, suggesting that HNRNPC may cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation. Our study also has certain limitations. For example, the data of the experimental group and the validation group come from different cell types, and the data of the experimental group involve individuals with G2019S LRRK2 mutations. In addition, due to the low expression of HNRNPC in PC12 cells, we used the method of overexpressing this gene to study its function. All these factors may cause our conclusions to be biased. Therefore, more research is still needed to corroborate it in the future. |
| format | Article |
| id | doaj-art-ae3df888c623468094390a17ba804aae |
| institution | Kabale University |
| issn | 2042-0080 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Parkinson's Disease |
| spelling | doaj-art-ae3df888c623468094390a17ba804aae2025-02-03T01:20:38ZengWileyParkinson's Disease2042-00802021-01-01202110.1155/2021/9919129Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s DiseaseWei Quan0Jia Li1Li Liu2Qinghui Zhang3Yidan Qin4Xiaochen Pei5Jiajun Chen6Department of NeurologyDepartment of NeurologyDepartment of NeurologyDepartment of NeurologyDepartment of NeurologyDepartment of NeurologyDepartment of NeurologyThis study aimed to explore the N6-methyladenosine (m6A) modification genes involved in the pathogenesis of Parkinson’s disease (PD) through data analysis of the two data sets GSE120306 and GSE22491 in the GEO database and further explore its influence on cell phenotype in PD. We analyzed the differentially expressed genes and function enrichment analysis of the two sets of data and found that the expression of the m6A-modification gene HNRNPC was significantly downregulated in the PD group, and it played an important role in DNA metabolism, RNA metabolism, and RNA processing and may be involved in PD. Then, we constructed the HNRNPC differential expression cell line to study the role of this gene in the pathogenesis of PD. The results showed that overexpression of HNRNPC can promote the proliferation of PC12 cells, inhibit their apoptosis, and inhibit the expression of inflammatory factors IFN-β, IL-6, and TNF-α, suggesting that HNRNPC may cause PD by inhibiting the proliferation of dopaminergic nerve cells, promoting their apoptosis, and causing immune inflammation. Our study also has certain limitations. For example, the data of the experimental group and the validation group come from different cell types, and the data of the experimental group involve individuals with G2019S LRRK2 mutations. In addition, due to the low expression of HNRNPC in PC12 cells, we used the method of overexpressing this gene to study its function. All these factors may cause our conclusions to be biased. Therefore, more research is still needed to corroborate it in the future.http://dx.doi.org/10.1155/2021/9919129 |
| spellingShingle | Wei Quan Jia Li Li Liu Qinghui Zhang Yidan Qin Xiaochen Pei Jiajun Chen Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease Parkinson's Disease |
| title | Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease |
| title_full | Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease |
| title_fullStr | Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease |
| title_full_unstemmed | Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease |
| title_short | Influence of N6-Methyladenosine Modification Gene HNRNPC on Cell Phenotype in Parkinson’s Disease |
| title_sort | influence of n6 methyladenosine modification gene hnrnpc on cell phenotype in parkinson s disease |
| url | http://dx.doi.org/10.1155/2021/9919129 |
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