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Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice
INTRODUCTION: Age is an established risk factor for neurodegenerative disorders. Aging-related cognitive decline is a common cause of memory impairment in aging individuals, in which hippocampal synaptic plasticity and hippocampus-dependent memory formation are damaged. Circular RNAs (circRNAs) have...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756809/ https://www.ncbi.nlm.nih.gov/pubmed/36533129 http://dx.doi.org/10.3389/fnmol.2022.1037912 |
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author | Li, Yibo Wang, Hongfang Gao, Yanjing Zhang, Runjiao Liu, Qing Xie, Wenmeng Liu, Ziyu Geng, Dandan Wang, Lei |
author_facet | Li, Yibo Wang, Hongfang Gao, Yanjing Zhang, Runjiao Liu, Qing Xie, Wenmeng Liu, Ziyu Geng, Dandan Wang, Lei |
author_sort | Li, Yibo |
collection | PubMed |
description | INTRODUCTION: Age is an established risk factor for neurodegenerative disorders. Aging-related cognitive decline is a common cause of memory impairment in aging individuals, in which hippocampal synaptic plasticity and hippocampus-dependent memory formation are damaged. Circular RNAs (circRNAs) have been reported in many cognitive disorders, but their role in aging-related memory impairment is unclear. Methods: In this study, we aimed to investigate the effects of circ-Vps41 on aging-related hippocampus-dependent memory impairment and explore the potential mechanisms. Here, D-galactose was used to produce a conventional aging model resulting in memory dysfunction. RESULTS: Circ-Vps41 was significantly downregulated in D-galactose-induced aging in vitro and in vivo. The overexpression of circ-Vps41 could upregulate synaptophysin (Syp), thereby promoting the synaptic plasticity and alleviating cognitive impairment in aging mice. Mechanistically, we found that circ-Vps41 upregulated Syp expression by physically binding to miR-24-3p. Moreover, the miR-24-3p mimics reversed the circ-Vps41 overexpression-induced increase in Syp expression. DISCUSSION: Overexpression of circ-Vps41 alleviated the synaptic plasticity and memory dysfunction via the miR-24-3p/Syp axis. These findings revealed circ-Vps41 regulatory network and provided new insights into its potential mechanisms for improving aging-related learning and memory impairment. |
format | Online Article Text |
id | pubmed-9756809 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-97568092022-12-17 Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice Li, Yibo Wang, Hongfang Gao, Yanjing Zhang, Runjiao Liu, Qing Xie, Wenmeng Liu, Ziyu Geng, Dandan Wang, Lei Front Mol Neurosci Molecular Neuroscience INTRODUCTION: Age is an established risk factor for neurodegenerative disorders. Aging-related cognitive decline is a common cause of memory impairment in aging individuals, in which hippocampal synaptic plasticity and hippocampus-dependent memory formation are damaged. Circular RNAs (circRNAs) have been reported in many cognitive disorders, but their role in aging-related memory impairment is unclear. Methods: In this study, we aimed to investigate the effects of circ-Vps41 on aging-related hippocampus-dependent memory impairment and explore the potential mechanisms. Here, D-galactose was used to produce a conventional aging model resulting in memory dysfunction. RESULTS: Circ-Vps41 was significantly downregulated in D-galactose-induced aging in vitro and in vivo. The overexpression of circ-Vps41 could upregulate synaptophysin (Syp), thereby promoting the synaptic plasticity and alleviating cognitive impairment in aging mice. Mechanistically, we found that circ-Vps41 upregulated Syp expression by physically binding to miR-24-3p. Moreover, the miR-24-3p mimics reversed the circ-Vps41 overexpression-induced increase in Syp expression. DISCUSSION: Overexpression of circ-Vps41 alleviated the synaptic plasticity and memory dysfunction via the miR-24-3p/Syp axis. These findings revealed circ-Vps41 regulatory network and provided new insights into its potential mechanisms for improving aging-related learning and memory impairment. Frontiers Media S.A. 2022-12-02 /pmc/articles/PMC9756809/ /pubmed/36533129 http://dx.doi.org/10.3389/fnmol.2022.1037912 Text en Copyright © 2022 Li, Wang, Gao, Zhang, Liu, Xie, Liu, Geng and Wang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Molecular Neuroscience Li, Yibo Wang, Hongfang Gao, Yanjing Zhang, Runjiao Liu, Qing Xie, Wenmeng Liu, Ziyu Geng, Dandan Wang, Lei Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title | Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title_full | Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title_fullStr | Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title_full_unstemmed | Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title_short | Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice |
title_sort | circ-vps41 positively modulates syp and its overexpression improves memory ability in aging mice |
topic | Molecular Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9756809/ https://www.ncbi.nlm.nih.gov/pubmed/36533129 http://dx.doi.org/10.3389/fnmol.2022.1037912 |
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