MicroRNA-125a-3p通过MAPK通路调节阿尔茨海默病中的淀粉样蛋白β-蛋白。

IF 1.8 4区 医学 Q3 CLINICAL NEUROLOGY
Xi-Chen Zhu, Meng-Zhuo Zhu, Jing Lu, Qing-Yu Yao, Jia-Wei Hu, Wen-Jun Long, Sha-Sha Ruan, Wen-Zhuo Dai, Rong Li
{"title":"MicroRNA-125a-3p通过MAPK通路调节阿尔茨海默病中的淀粉样蛋白β-蛋白。","authors":"Xi-Chen Zhu, Meng-Zhuo Zhu, Jing Lu, Qing-Yu Yao, Jia-Wei Hu, Wen-Jun Long, Sha-Sha Ruan, Wen-Zhuo Dai, Rong Li","doi":"10.2174/1567205020666230913105811","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>MicroRNA (miR)-125a-3p is reported to play an important role in some central nervous system diseases, such as Alzheimer's disease (AD). However, a study has not been conducted on the mechanism of miR-125a-3p in the pathological process of AD.</p><p><strong>Methods: </strong>First, we assessed the expression of miR-125a-3p in AD cohort. Subsequently, we altered the expressions of miR-125a-3p to assess its role in cell viability, cell apoptosis, amyloid-β (Aβ) metabolism, and synaptic activity. Finally, we identified its potential mechanism underlying AD pathology.</p><p><strong>Results: </strong>This study unveiled the potential function of miR-125a-3p through modulating amyloid precursor protein processing. Additionally, miR-125a-3p influenced cell survival and activated synaptic expression through the modulation of Aβ metabolism in the mitogen-activated protein kinase (MAPK) pathway via fibroblast growth factor receptor 2.</p><p><strong>Conclusion: </strong>Our study indicates that targeting miR-125a-3p may be an applicable therapy for AD in the future. However, more in vitro and in vivo studies with more samples are needed to confirm these results.</p>","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":null,"pages":null},"PeriodicalIF":1.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MicroRNA-125a-3p Modulate Amyloid β-Protein through the MAPK Pathway in Alzheimer's Disease.\",\"authors\":\"Xi-Chen Zhu, Meng-Zhuo Zhu, Jing Lu, Qing-Yu Yao, Jia-Wei Hu, Wen-Jun Long, Sha-Sha Ruan, Wen-Zhuo Dai, Rong Li\",\"doi\":\"10.2174/1567205020666230913105811\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>MicroRNA (miR)-125a-3p is reported to play an important role in some central nervous system diseases, such as Alzheimer's disease (AD). However, a study has not been conducted on the mechanism of miR-125a-3p in the pathological process of AD.</p><p><strong>Methods: </strong>First, we assessed the expression of miR-125a-3p in AD cohort. Subsequently, we altered the expressions of miR-125a-3p to assess its role in cell viability, cell apoptosis, amyloid-β (Aβ) metabolism, and synaptic activity. Finally, we identified its potential mechanism underlying AD pathology.</p><p><strong>Results: </strong>This study unveiled the potential function of miR-125a-3p through modulating amyloid precursor protein processing. Additionally, miR-125a-3p influenced cell survival and activated synaptic expression through the modulation of Aβ metabolism in the mitogen-activated protein kinase (MAPK) pathway via fibroblast growth factor receptor 2.</p><p><strong>Conclusion: </strong>Our study indicates that targeting miR-125a-3p may be an applicable therapy for AD in the future. However, more in vitro and in vivo studies with more samples are needed to confirm these results.</p>\",\"PeriodicalId\":10810,\"journal\":{\"name\":\"Current Alzheimer research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current Alzheimer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/1567205020666230913105811\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Alzheimer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1567205020666230913105811","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:据报道,MicroRNA (miR)-125a-3p在阿尔茨海默病(AD)等中枢神经系统疾病中发挥重要作用。然而,miR-125a-3p在AD病理过程中的作用机制尚未有研究。方法:首先,我们评估miR-125a-3p在AD队列中的表达。随后,我们改变了miR-125a-3p的表达,以评估其在细胞活力、细胞凋亡、淀粉样蛋白-β (Aβ)代谢和突触活性中的作用。最后,我们确定了其潜在的AD病理机制。结果:本研究揭示了miR-125a-3p通过调节淀粉样蛋白前体蛋白加工的潜在功能。此外,miR-125a-3p通过成纤维细胞生长因子受体2调节丝裂原活化蛋白激酶(MAPK)通路中的Aβ代谢,从而影响细胞存活并激活突触表达。结论:我们的研究表明,靶向miR-125a-3p可能是未来治疗AD的一种适用的治疗方法。然而,需要更多样本的体外和体内研究来证实这些结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MicroRNA-125a-3p Modulate Amyloid β-Protein through the MAPK Pathway in Alzheimer's Disease.

Background: MicroRNA (miR)-125a-3p is reported to play an important role in some central nervous system diseases, such as Alzheimer's disease (AD). However, a study has not been conducted on the mechanism of miR-125a-3p in the pathological process of AD.

Methods: First, we assessed the expression of miR-125a-3p in AD cohort. Subsequently, we altered the expressions of miR-125a-3p to assess its role in cell viability, cell apoptosis, amyloid-β (Aβ) metabolism, and synaptic activity. Finally, we identified its potential mechanism underlying AD pathology.

Results: This study unveiled the potential function of miR-125a-3p through modulating amyloid precursor protein processing. Additionally, miR-125a-3p influenced cell survival and activated synaptic expression through the modulation of Aβ metabolism in the mitogen-activated protein kinase (MAPK) pathway via fibroblast growth factor receptor 2.

Conclusion: Our study indicates that targeting miR-125a-3p may be an applicable therapy for AD in the future. However, more in vitro and in vivo studies with more samples are needed to confirm these results.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Current Alzheimer research
Current Alzheimer research 医学-神经科学
CiteScore
4.00
自引率
4.80%
发文量
64
审稿时长
4-8 weeks
期刊介绍: Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信