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Integrated analysis of the lncRNA-associated ceRNA network in Alzheimer's disease.
Cai, Hong-Yan; Chen, Si-Ru; Wang, Yu; Jiao, Juan-Juan; Qiao, Jun; Hölscher, Christian; Wang, Zhao-Jun; Zhang, Sheng-Xiao; Wu, Mei-Na.
Afiliação
  • Cai HY; Department of Microbiology and Immunology, Shanxi Medical University, Taiyuan, China; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, Taiyuan, China; Key Laboratory of Cellular Physiology, Shanxi Province, China. Electronic address: yancai1@163.com.
  • Chen SR; Department of Microbiology and Immunology, Shanxi Medical University, Taiyuan, China. Electronic address: chensiru960713@126.com.
  • Wang Y; Department of Microbiology and Immunology, Shanxi Medical University, Taiyuan, China. Electronic address: 765178069@qq.com.
  • Jiao JJ; Department of Physiology, Shanxi Medical University, Taiyuan, China. Electronic address: 1182239674@qq.com.
  • Qiao J; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, Taiyuan, China; Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. Electronic address: qiaojunys@163.com.
  • Hölscher C; Academy of Chinese Medical Science, Henan university of Chinese medicine, Zhengzhou, China. Electronic address: c.holscher@hactcm.edu.cn.
  • Wang ZJ; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, Taiyuan, China; Key Laboratory of Cellular Physiology, Shanxi Province, China; Department of Physiology, Shanxi Medical University, Taiyuan, China. Electronic address: wzhaojun1025@126.com.
  • Zhang SX; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, Taiyuan, China; Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. Electronic address: shengxiao_zhang@163.com.
  • Wu MN; Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, Taiyuan, China; Key Laboratory of Cellular Physiology, Shanxi Province, China; Department of Physiology, Shanxi Medical University, Taiyuan, China. Electronic address: wmna@163.com.
Gene ; 876: 147484, 2023 Aug 05.
Article em En | MEDLINE | ID: mdl-37187245
ABSTRACT
Alzheimer's disease (AD) is a progressive neurodegenerative disease that worsens with age. Long non-coding RNAs (lncRNAs) dysregulation and its associated competing endogenous RNA (ceRNA) network have a potential connection with the occurrence and development of AD. A total of 358 differentially expressed genes (DEGs) were screened via RNA sequencing, including 302 differentially expressed mRNAs (DEmRNAs) and 56 differential expressed lncRNAs (DElncRNAs). Anti-sense lncRNA is the main type of DElncRNA, which plays a major role in the cis and trans regulation. The constructed ceRNA network consisted of 4 lncRNAs (NEAT1, LINC00365, FBXL19-AS1, RAI1-AS1719) and 4 microRNAs (miRNAs) (HSA-Mir-27a-3p, HSA-Mir-20b-5p, HSA-Mir-17-5p, HSA-Mir-125b-5p), and 2 mRNAs (MKNK2, F3). Functional enrichment analysis revealed that DEmRNAs are involved in related biological functions of AD. The co-expressed DEmRNAs (DNAH11, HGFAC, TJP3, TAC1, SPTSSB, SOWAHB, RGS4, ADCYAP1) of humans and mice were screened and verified by real-time quantitative polymerase chain reaction (qRT-PCR). In this study, we analyzed the expression profile of human AD-related lncRNA genes, constructed a ceRNA network, and performed functional enrichment analysis of DEmRNAs between human and mice. The obtained gene regulatory networks and target genes can be used to further analyze AD-related pathological mechanisms to optimize AD diagnosis and treatment.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / MicroRNAs / Doença de Alzheimer / RNA Longo não Codificante Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / MicroRNAs / Doença de Alzheimer / RNA Longo não Codificante Idioma: En Ano de publicação: 2023 Tipo de documento: Article