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Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics
AIMS/INTRODUCTION: Body aging is a universal biological process. With aging, cells undergo a series of physiological changes. The main feature is cell proliferation decline, although the cells still have normal functions. Pancreatic β‐cells are no exception. However, the physiological senescence of...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8504912/ https://www.ncbi.nlm.nih.gov/pubmed/34003589 http://dx.doi.org/10.1111/jdi.13579 |
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author | Zheng, Zeyu Zhan, Qiufeng Chen, Ayun Yu, Zhen Chen, Gang |
author_facet | Zheng, Zeyu Zhan, Qiufeng Chen, Ayun Yu, Zhen Chen, Gang |
author_sort | Zheng, Zeyu |
collection | PubMed |
description | AIMS/INTRODUCTION: Body aging is a universal biological process. With aging, cells undergo a series of physiological changes. The main feature is cell proliferation decline, although the cells still have normal functions. Pancreatic β‐cells are no exception. However, the physiological senescence of β‐cells, and the resulting function and transcriptome changes have rarely attracted attention. The specific senescence phenotype of β‐cells remains unknown. MATERIALS AND METHODS: Pancreatic samples from three female C57BL/6 mice with aged 2.5 months (young) mice and 20 months (old) were digested to a single‐cell suspension and analyzed, with 10× Genomics single‐cell ribonucleic acid sequencing, β‐cells were determined by biosynthesis analysis, and differences between old and young mice were identified. RESULTS: A total of 47 differential genes with significant and statistical significance were screened in β‐cells (fold change >1.5, P < 0.05). In old mice, 27 genes were upregulated and 20 genes were downregulated. Genes Mt1, Mt2, Pyy, Gcg and Pnlip, and mitochondrial genes mt‐Nd1, mt‐Nd3, mt‐Co1, mt‐Co2 and mt‐Co3 were found to be involved in cellular senescence. Transcription factors Jund and Fos were important regulators of senescence. CONCLUSIONS: An overall difference was found between the pancreatic β‐cells of old and young mice. Transcription factors facilitate transitions between pancreatic β‐cells. These findings are worthy of deep exploration, and provide new resources and directions for the research of pancreatic aging in mice. |
format | Online Article Text |
id | pubmed-8504912 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85049122021-10-18 Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics Zheng, Zeyu Zhan, Qiufeng Chen, Ayun Yu, Zhen Chen, Gang J Diabetes Investig Original Articles AIMS/INTRODUCTION: Body aging is a universal biological process. With aging, cells undergo a series of physiological changes. The main feature is cell proliferation decline, although the cells still have normal functions. Pancreatic β‐cells are no exception. However, the physiological senescence of β‐cells, and the resulting function and transcriptome changes have rarely attracted attention. The specific senescence phenotype of β‐cells remains unknown. MATERIALS AND METHODS: Pancreatic samples from three female C57BL/6 mice with aged 2.5 months (young) mice and 20 months (old) were digested to a single‐cell suspension and analyzed, with 10× Genomics single‐cell ribonucleic acid sequencing, β‐cells were determined by biosynthesis analysis, and differences between old and young mice were identified. RESULTS: A total of 47 differential genes with significant and statistical significance were screened in β‐cells (fold change >1.5, P < 0.05). In old mice, 27 genes were upregulated and 20 genes were downregulated. Genes Mt1, Mt2, Pyy, Gcg and Pnlip, and mitochondrial genes mt‐Nd1, mt‐Nd3, mt‐Co1, mt‐Co2 and mt‐Co3 were found to be involved in cellular senescence. Transcription factors Jund and Fos were important regulators of senescence. CONCLUSIONS: An overall difference was found between the pancreatic β‐cells of old and young mice. Transcription factors facilitate transitions between pancreatic β‐cells. These findings are worthy of deep exploration, and provide new resources and directions for the research of pancreatic aging in mice. John Wiley and Sons Inc. 2021-06-25 2021-10 /pmc/articles/PMC8504912/ /pubmed/34003589 http://dx.doi.org/10.1111/jdi.13579 Text en © 2021 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Zheng, Zeyu Zhan, Qiufeng Chen, Ayun Yu, Zhen Chen, Gang Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title | Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title_full | Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title_fullStr | Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title_full_unstemmed | Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title_short | Islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
title_sort | islet β‐cells physiological difference study of old and young mice based on single‐cell transcriptomics |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8504912/ https://www.ncbi.nlm.nih.gov/pubmed/34003589 http://dx.doi.org/10.1111/jdi.13579 |
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