TY - JOUR
T1 - MicroRNA and mRNA profiling of cerebral cortex in a transgenic mouse model of Alzheimer's disease by RNA sequencing
AU - Zeng, Li
AU - Jiang, Hai Lun
AU - Ashraf, Ghulam
AU - Li, Zhuo Rong
AU - Liu, Rui
N1 - Publisher Copyright:
© 2021 Wolters Kluwer Medknow Publications. All rights reserved.
PY - 2021/10
Y1 - 2021/10
N2 - In a previous study, we found that long non-coding genes in Alzheimer's disease (AD) are a result of endogenous gene disorders caused by the recruitment of microRNA (miRNA) and mRNA, and that miR-200a-3p and other representative miRNAs can mediate cognitive impairment and thus serve as new biomarkers for AD. In this study, we investigated the abnormal expression of miRNA and mRNA and the pathogenesis of AD at the epigenetic level. To this aim, we performed RNA sequencing and an integrative analysis of the cerebral cortex of the widely used amyloid precursor protein and presenilin-1 double transgenic mouse model of AD. Overall, 129 mRNAs and 68 miRNAs were aberrantly expressed. Among these, eight down-regulated miRNAs and seven up-regulated miRNAs appeared as promising noninvasive biomarkers and therapeutic targets. The main enriched signaling pathways involved mitogen-activated kinase protein, phosphatidylinositol 3-kinase-protein kinase B, mechanistic target of rapamycin kinase, forkhead box O, and autophagy. An miRNA-mRNA network between dysregulated miRNAs and corresponding target genes connected with AD progression was also constructed. These miRNAs and mRNAs are potential biomarkers and therapeutic targets for new treatment strategies, early diagnosis, and prevention of AD. The present results provide a novel perspective on the role of miRNAs and mRNAs in AD. This study was approved by the Experimental Animal Care and Use Committee of Institute of Medicinal Biotechnology of Beijing, China (approval No. IMB-201909-D6) on September 6, 2019.
AB - In a previous study, we found that long non-coding genes in Alzheimer's disease (AD) are a result of endogenous gene disorders caused by the recruitment of microRNA (miRNA) and mRNA, and that miR-200a-3p and other representative miRNAs can mediate cognitive impairment and thus serve as new biomarkers for AD. In this study, we investigated the abnormal expression of miRNA and mRNA and the pathogenesis of AD at the epigenetic level. To this aim, we performed RNA sequencing and an integrative analysis of the cerebral cortex of the widely used amyloid precursor protein and presenilin-1 double transgenic mouse model of AD. Overall, 129 mRNAs and 68 miRNAs were aberrantly expressed. Among these, eight down-regulated miRNAs and seven up-regulated miRNAs appeared as promising noninvasive biomarkers and therapeutic targets. The main enriched signaling pathways involved mitogen-activated kinase protein, phosphatidylinositol 3-kinase-protein kinase B, mechanistic target of rapamycin kinase, forkhead box O, and autophagy. An miRNA-mRNA network between dysregulated miRNAs and corresponding target genes connected with AD progression was also constructed. These miRNAs and mRNAs are potential biomarkers and therapeutic targets for new treatment strategies, early diagnosis, and prevention of AD. The present results provide a novel perspective on the role of miRNAs and mRNAs in AD. This study was approved by the Experimental Animal Care and Use Committee of Institute of Medicinal Biotechnology of Beijing, China (approval No. IMB-201909-D6) on September 6, 2019.
KW - 3′-untranslated region
KW - Alzheimer's disease
KW - biomarker
KW - cerebral cortex
KW - Gene Ontology
KW - high-throughput sequencing
KW - intracellular neurofibrillary tangles
KW - microtubule-associated protein
KW - miRNA-mRNA network
KW - presenilin 1
UR - http://www.scopus.com/inward/record.url?scp=85101996052&partnerID=8YFLogxK
U2 - 10.4103/1673-5374.308104
DO - 10.4103/1673-5374.308104
M3 - Article
AN - SCOPUS:85101996052
SN - 1673-5374
VL - 16
SP - 2099
EP - 2108
JO - Neural Regeneration Research
JF - Neural Regeneration Research
IS - 10
ER -