ArticleJournal of biomedical science2015
DNA methylation regulates mouse cardiac myofibril gene expression during heart development.
Article in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- The role of DNA methylation in syndromic and non-syndromic congenital heart disease.Clinical epigenetics · 2021Review
- Developmental plasticity of cardiac anoxia-tolerance in juvenile common snapping turtles ( Chelydra serpentina).Proceedings. Biological sciences · 2019Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt 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.
resultsThe 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.
conclusionOur 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.
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