{"title":"lncRNA SOX21-AS1通过表观遗传沉默SOCS3促进BV2细胞的激活并加重帕金森病的病情","authors":"Dan Feng, Yun Liu, Fangya Zuo, Fenfen Liu, Yuqi Liu, Yujie Wang, Lanlan Chen, Xiuhong Guo, Jinyong Tian","doi":"10.1159/000539784","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>LncRNAs perform a crucial impact on microglia's activation in Parkinson's disease (PD). Here, our purpose was to probe the function and involved mechanism of lncRNA SOX21-AS1 on microglial activation in PD.</p><p><strong>Methods: </strong>Mice were treated with MPTP, and BV2 cells were treated with LPS/ATP to build PD animal and cell models. Genes' expression was measured using RT-qPCR, immunoblotting, and IHC stain. ELISA was applied for testing inflammatory factors' levels. Cell viability and apoptosis were tested using kits. RIP and RNA pull-down assay were utilized for monitoring the bond of SOX21-AS1 to EZH2, and ChIP was applied for affirming the bond between EZH2 and SOCS3's promoter.</p><p><strong>Results: </strong>The expression of SOX21-AS1 and SOCS3 was abnormal in PD cell and animal models. Inhibition of SOX21-AS1 repressed LPS/ATP-induced activation in BV2 cells and nerve damage caused by activated BV2 cells, alleviating the pathological features of PD mice. Further studies found that SOX21-AS1 epigenetically inhibited SOCS3 by recruiting EZH2 to SOCS3 promoter. SOX21-AS1 overexpression partially offset the repressive impact of SOCS3 enhancement on BV2 cell activation and the protective effect on nerve cells.</p><p><strong>Conclusion: </strong>SOX21-AS1 enhances LPS/ATP-induced activation of BV2 cells and nerve damage caused by activated BV2 cells though recruiting EZH2 to SOCS3's promoter, thereby alleviating PD progression. Our research supplies new potential target for curing PD.</p>","PeriodicalId":12662,"journal":{"name":"Gerontology","volume":" ","pages":"1063-1073"},"PeriodicalIF":3.1000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA SOX21-AS1 Promotes Activation of BV2 Cells via Epigenetical Silencing of SOCS3 and Aggravates Parkinson's Disease.\",\"authors\":\"Dan Feng, Yun Liu, Fangya Zuo, Fenfen Liu, Yuqi Liu, Yujie Wang, Lanlan Chen, Xiuhong Guo, Jinyong Tian\",\"doi\":\"10.1159/000539784\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>LncRNAs perform a crucial impact on microglia's activation in Parkinson's disease (PD). Here, our purpose was to probe the function and involved mechanism of lncRNA SOX21-AS1 on microglial activation in PD.</p><p><strong>Methods: </strong>Mice were treated with MPTP, and BV2 cells were treated with LPS/ATP to build PD animal and cell models. Genes' expression was measured using RT-qPCR, immunoblotting, and IHC stain. ELISA was applied for testing inflammatory factors' levels. Cell viability and apoptosis were tested using kits. RIP and RNA pull-down assay were utilized for monitoring the bond of SOX21-AS1 to EZH2, and ChIP was applied for affirming the bond between EZH2 and SOCS3's promoter.</p><p><strong>Results: </strong>The expression of SOX21-AS1 and SOCS3 was abnormal in PD cell and animal models. Inhibition of SOX21-AS1 repressed LPS/ATP-induced activation in BV2 cells and nerve damage caused by activated BV2 cells, alleviating the pathological features of PD mice. Further studies found that SOX21-AS1 epigenetically inhibited SOCS3 by recruiting EZH2 to SOCS3 promoter. SOX21-AS1 overexpression partially offset the repressive impact of SOCS3 enhancement on BV2 cell activation and the protective effect on nerve cells.</p><p><strong>Conclusion: </strong>SOX21-AS1 enhances LPS/ATP-induced activation of BV2 cells and nerve damage caused by activated BV2 cells though recruiting EZH2 to SOCS3's promoter, thereby alleviating PD progression. Our research supplies new potential target for curing PD.</p>\",\"PeriodicalId\":12662,\"journal\":{\"name\":\"Gerontology\",\"volume\":\" \",\"pages\":\"1063-1073\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gerontology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000539784\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/7/24 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gerontology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000539784","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/24 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
LncRNA SOX21-AS1 Promotes Activation of BV2 Cells via Epigenetical Silencing of SOCS3 and Aggravates Parkinson's Disease.
Background: LncRNAs perform a crucial impact on microglia's activation in Parkinson's disease (PD). Here, our purpose was to probe the function and involved mechanism of lncRNA SOX21-AS1 on microglial activation in PD.
Methods: Mice were treated with MPTP, and BV2 cells were treated with LPS/ATP to build PD animal and cell models. Genes' expression was measured using RT-qPCR, immunoblotting, and IHC stain. ELISA was applied for testing inflammatory factors' levels. Cell viability and apoptosis were tested using kits. RIP and RNA pull-down assay were utilized for monitoring the bond of SOX21-AS1 to EZH2, and ChIP was applied for affirming the bond between EZH2 and SOCS3's promoter.
Results: The expression of SOX21-AS1 and SOCS3 was abnormal in PD cell and animal models. Inhibition of SOX21-AS1 repressed LPS/ATP-induced activation in BV2 cells and nerve damage caused by activated BV2 cells, alleviating the pathological features of PD mice. Further studies found that SOX21-AS1 epigenetically inhibited SOCS3 by recruiting EZH2 to SOCS3 promoter. SOX21-AS1 overexpression partially offset the repressive impact of SOCS3 enhancement on BV2 cell activation and the protective effect on nerve cells.
Conclusion: SOX21-AS1 enhances LPS/ATP-induced activation of BV2 cells and nerve damage caused by activated BV2 cells though recruiting EZH2 to SOCS3's promoter, thereby alleviating PD progression. Our research supplies new potential target for curing PD.
期刊介绍：
In view of the ever-increasing fraction of elderly people, understanding the mechanisms of aging and age-related diseases has become a matter of urgent necessity. ''Gerontology'', the oldest journal in the field, responds to this need by drawing topical contributions from multiple disciplines to support the fundamental goals of extending active life and enhancing its quality. The range of papers is classified into four sections. In the Clinical Section, the aetiology, pathogenesis, prevention and treatment of agerelated diseases are discussed from a gerontological rather than a geriatric viewpoint. The Experimental Section contains up-to-date contributions from basic gerontological research. Papers dealing with behavioural development and related topics are placed in the Behavioural Science Section. Basic aspects of regeneration in different experimental biological systems as well as in the context of medical applications are dealt with in a special section that also contains information on technological advances for the elderly. Providing a primary source of high-quality papers covering all aspects of aging in humans and animals, ''Gerontology'' serves as an ideal information tool for all readers interested in the topic of aging from a broad perspective.
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