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Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy
AIM: To analyze and compare the mRNA N(6)-methyladenosine modifications in transverse aortic constriction induced mice hearts and normal mice hearts. MATERIALS AND METHODS: Colorimetric quantification was used to probe the changes in m(6)A modifications in the total RNA. The expression of m(6)A-rela...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9373449/ https://www.ncbi.nlm.nih.gov/pubmed/35953789 http://dx.doi.org/10.1186/s12864-022-08833-w |
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author | Li, Weidong Xing, Chenxv Bao, Limeng Han, Shengna Luo, Tianxia Wang, Zhiju Fan, Hongkun |
author_facet | Li, Weidong Xing, Chenxv Bao, Limeng Han, Shengna Luo, Tianxia Wang, Zhiju Fan, Hongkun |
author_sort | Li, Weidong |
collection | PubMed |
description | AIM: To analyze and compare the mRNA N(6)-methyladenosine modifications in transverse aortic constriction induced mice hearts and normal mice hearts. MATERIALS AND METHODS: Colorimetric quantification was used to probe the changes in m(6)A modifications in the total RNA. The expression of m(6)A-related enzymes was analyzed via qRT-PCR and western blotting. RNA-seq and MeRIP-seq were performed to identify genes with differences in m(6)A modifications or expression in the transcriptome profile. RESULTS: Compared with the control group, the TAC group exhibited higher m(6)A methylation levels. FTO and WTAP were downregulated after TAC, while METTL3 was significantly downregulated at the protein level. MeRIP-seq revealed that 1179 m(6)A peaks were upmethylated and 733 m(6)A peaks were downmethylated, and biological analysis of these genes exhibited a strong relationship with heart function. CONCLUSION: Our findings provide novel information regarding m(6)A modification and gene expression changes in cardiac hypertrophy, which may be fundamental for further research. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-022-08833-w. |
format | Online Article Text |
id | pubmed-9373449 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-93734492022-08-13 Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy Li, Weidong Xing, Chenxv Bao, Limeng Han, Shengna Luo, Tianxia Wang, Zhiju Fan, Hongkun BMC Genomics Research AIM: To analyze and compare the mRNA N(6)-methyladenosine modifications in transverse aortic constriction induced mice hearts and normal mice hearts. MATERIALS AND METHODS: Colorimetric quantification was used to probe the changes in m(6)A modifications in the total RNA. The expression of m(6)A-related enzymes was analyzed via qRT-PCR and western blotting. RNA-seq and MeRIP-seq were performed to identify genes with differences in m(6)A modifications or expression in the transcriptome profile. RESULTS: Compared with the control group, the TAC group exhibited higher m(6)A methylation levels. FTO and WTAP were downregulated after TAC, while METTL3 was significantly downregulated at the protein level. MeRIP-seq revealed that 1179 m(6)A peaks were upmethylated and 733 m(6)A peaks were downmethylated, and biological analysis of these genes exhibited a strong relationship with heart function. CONCLUSION: Our findings provide novel information regarding m(6)A modification and gene expression changes in cardiac hypertrophy, which may be fundamental for further research. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-022-08833-w. BioMed Central 2022-08-11 /pmc/articles/PMC9373449/ /pubmed/35953789 http://dx.doi.org/10.1186/s12864-022-08833-w Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Li, Weidong Xing, Chenxv Bao, Limeng Han, Shengna Luo, Tianxia Wang, Zhiju Fan, Hongkun Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title | Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title_full | Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title_fullStr | Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title_full_unstemmed | Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title_short | Comprehensive analysis of RNA m6A methylation in pressure overload-induced cardiac hypertrophy |
title_sort | comprehensive analysis of rna m6a methylation in pressure overload-induced cardiac hypertrophy |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9373449/ https://www.ncbi.nlm.nih.gov/pubmed/35953789 http://dx.doi.org/10.1186/s12864-022-08833-w |
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