Cargando…
DNA methylation regulates mouse cardiac myofibril gene expression during heart development
BACKGROUND: It is well known that epigenetic modifications play an important role in controlling the regulation of gene expression during the development. Our previous studies have demonstrated that the expression of fetal troponin I gene (also called slow skeletal troponin I, ssTnI) is predominated...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609054/ https://www.ncbi.nlm.nih.gov/pubmed/26475623 http://dx.doi.org/10.1186/s12929-015-0203-6 |
_version_ | 1782395756931448832 |
---|---|
author | Xu, Yang Liu, Lingjuan Pan, Bo Zhu, Jing Nan, Changlong Huang, Xupei Tian, Jie |
author_facet | Xu, Yang Liu, Lingjuan Pan, Bo Zhu, Jing Nan, Changlong Huang, Xupei Tian, Jie |
author_sort | Xu, Yang |
collection | PubMed |
description | BACKGROUND: It is well known that epigenetic modifications play an important role in controlling the regulation of gene expression during the development. Our previous studies have demonstrated that the expression of fetal troponin I gene (also called slow skeletal troponin I, ssTnI) is predominated in the fetal stage, reduced after birth and disappeared in the adulthood. The mechanism underlying the developmentally related ssTnI gene regulation is not clear. In this study, we have explored the epigenetic role of DNA methylation in the regulation of ssTnI expression in the heart during the development. RESULTS: The DNA methylation levels of CpG island and CpG dinucleotides region were detected using methylation specific PCR (MSP) and bisulfite sequence PCR (BSP) in 2000 bp upstream and 100 bp upstream of ssTnI gene promoter. Real time RT-PCR and Western blot were used to detect ssTnI mRNA and protein expression levels. We found that DNA methylation levels of the CpG dinucleotides region in ssTnI gene promoter were increased with the development, corresponding to a decreased expression of ssTnI gene in mouse heart. However the DNA methylation levels of CpG islands in this gene were not changed during the development. Application of a methylation inhibitor, 5-Azacytidine, in cultured myocardial cells partially prevented the decline of ssTnI expression. CONCLUSION: Our results indicate that DNA methylation, as an epigenetic intervention, plays a role in the regulation of the fetal TnI gene expression in the heat during the development. |
format | Online Article Text |
id | pubmed-4609054 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-46090542015-10-18 DNA methylation regulates mouse cardiac myofibril gene expression during heart development Xu, Yang Liu, Lingjuan Pan, Bo Zhu, Jing Nan, Changlong Huang, Xupei Tian, Jie J Biomed Sci Research BACKGROUND: It is well known that epigenetic modifications play an important role in controlling the regulation of gene expression during the development. Our previous studies have demonstrated that the expression of fetal troponin I gene (also called slow skeletal troponin I, ssTnI) is predominated in the fetal stage, reduced after birth and disappeared in the adulthood. The mechanism underlying the developmentally related ssTnI gene regulation is not clear. In this study, we have explored the epigenetic role of DNA methylation in the regulation of ssTnI expression in the heart during the development. RESULTS: The DNA methylation levels of CpG island and CpG dinucleotides region were detected using methylation specific PCR (MSP) and bisulfite sequence PCR (BSP) in 2000 bp upstream and 100 bp upstream of ssTnI gene promoter. Real time RT-PCR and Western blot were used to detect ssTnI mRNA and protein expression levels. We found that DNA methylation levels of the CpG dinucleotides region in ssTnI gene promoter were increased with the development, corresponding to a decreased expression of ssTnI gene in mouse heart. However the DNA methylation levels of CpG islands in this gene were not changed during the development. Application of a methylation inhibitor, 5-Azacytidine, in cultured myocardial cells partially prevented the decline of ssTnI expression. CONCLUSION: Our results indicate that DNA methylation, as an epigenetic intervention, plays a role in the regulation of the fetal TnI gene expression in the heat during the development. BioMed Central 2015-10-17 /pmc/articles/PMC4609054/ /pubmed/26475623 http://dx.doi.org/10.1186/s12929-015-0203-6 Text en © Xu et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Xu, Yang Liu, Lingjuan Pan, Bo Zhu, Jing Nan, Changlong Huang, Xupei Tian, Jie DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title | DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title_full | DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title_fullStr | DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title_full_unstemmed | DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title_short | DNA methylation regulates mouse cardiac myofibril gene expression during heart development |
title_sort | dna methylation regulates mouse cardiac myofibril gene expression during heart development |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609054/ https://www.ncbi.nlm.nih.gov/pubmed/26475623 http://dx.doi.org/10.1186/s12929-015-0203-6 |
work_keys_str_mv | AT xuyang dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT liulingjuan dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT panbo dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT zhujing dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT nanchanglong dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT huangxupei dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment AT tianjie dnamethylationregulatesmousecardiacmyofibrilgeneexpressionduringheartdevelopment |