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Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats
BACKGROUND: Diabetes is a chronic metabolic disease and an independent risk factor for cognitive damage. Non-protein coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are involved in various pathophysiological conditions. METHODS: In this study, cognitive impairment was i...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267322/ https://www.ncbi.nlm.nih.gov/pubmed/34277765 http://dx.doi.org/10.21037/atm-21-2016 |
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author | Peng, Wenfang Xu, Bojin Ge, Xiaoxu Du, Juan Xi, Liuqing Xia, Lili Wang, Qianqian Huang, Shan |
author_facet | Peng, Wenfang Xu, Bojin Ge, Xiaoxu Du, Juan Xi, Liuqing Xia, Lili Wang, Qianqian Huang, Shan |
author_sort | Peng, Wenfang |
collection | PubMed |
description | BACKGROUND: Diabetes is a chronic metabolic disease and an independent risk factor for cognitive damage. Non-protein coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are involved in various pathophysiological conditions. METHODS: In this study, cognitive impairment was induced in diabetics rats by streptozotocin (STZ) injection, and the differential lncRNAs and mRNAs in rat hippocampal tissue between control and STZ-treated groups were analyzed with microarray. RESULTS: In the hippocampus of STZ-treated diabetic rats, lncRNA Vof-16, and Gnb3 mRNA were significantly upregulated and silicon analysis showed that Vof-16 and miR-205 share the same miRNA response element (MRE). In addition, the overexpression of Vof-16 in primary hippocampal neurons inhibited the expression of miR-205, and vice versa. Dual luciferase assay verified the binding between Vof-16 and miR-205, and Vof-16 was seen to promote the proliferation of primary hippocampal neurons via sponging miR-205. Silicon analysis predicted that miR-205 could bind with Gnb3, which was verified with dual luciferase assay, and the overexpression of miR-205 could inhibit the protein level of Gnb3, which could be rescued by co-expression with Vof-16. In conclusion, lncRNA Vof-16 regulated Gnb3 expression by competitively binding to miR-205. CONCLUSIONS: These results provided a novel regulation axis for the pathogenesis of STZ-induced diabetes. |
format | Online Article Text |
id | pubmed-8267322 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-82673222021-07-16 Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats Peng, Wenfang Xu, Bojin Ge, Xiaoxu Du, Juan Xi, Liuqing Xia, Lili Wang, Qianqian Huang, Shan Ann Transl Med Original Article BACKGROUND: Diabetes is a chronic metabolic disease and an independent risk factor for cognitive damage. Non-protein coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are involved in various pathophysiological conditions. METHODS: In this study, cognitive impairment was induced in diabetics rats by streptozotocin (STZ) injection, and the differential lncRNAs and mRNAs in rat hippocampal tissue between control and STZ-treated groups were analyzed with microarray. RESULTS: In the hippocampus of STZ-treated diabetic rats, lncRNA Vof-16, and Gnb3 mRNA were significantly upregulated and silicon analysis showed that Vof-16 and miR-205 share the same miRNA response element (MRE). In addition, the overexpression of Vof-16 in primary hippocampal neurons inhibited the expression of miR-205, and vice versa. Dual luciferase assay verified the binding between Vof-16 and miR-205, and Vof-16 was seen to promote the proliferation of primary hippocampal neurons via sponging miR-205. Silicon analysis predicted that miR-205 could bind with Gnb3, which was verified with dual luciferase assay, and the overexpression of miR-205 could inhibit the protein level of Gnb3, which could be rescued by co-expression with Vof-16. In conclusion, lncRNA Vof-16 regulated Gnb3 expression by competitively binding to miR-205. CONCLUSIONS: These results provided a novel regulation axis for the pathogenesis of STZ-induced diabetes. AME Publishing Company 2021-06 /pmc/articles/PMC8267322/ /pubmed/34277765 http://dx.doi.org/10.21037/atm-21-2016 Text en 2021 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) . |
spellingShingle | Original Article Peng, Wenfang Xu, Bojin Ge, Xiaoxu Du, Juan Xi, Liuqing Xia, Lili Wang, Qianqian Huang, Shan Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title | Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title_full | Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title_fullStr | Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title_full_unstemmed | Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title_short | Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
title_sort | vof16-mir-205-gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267322/ https://www.ncbi.nlm.nih.gov/pubmed/34277765 http://dx.doi.org/10.21037/atm-21-2016 |
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