From: The role of DNA methylation in syndromic and non-syndromic congenital heart disease
Study (reference) | Study population Sample type | Cohort | Sample | Methylation measures | DNA methylation change |
---|---|---|---|---|---|
[100] | Heart tissue (mouse) | Healthy | E11.5, E14.5 (n = 3 per group) | Genome‐wide DNA methylation profiling using MSFE/MPS | Global methylation in developing hearts remained stable between E11.5 and E14.5, a small fraction AGCT sites exhibited differential methylation, which were enriched in genes involved in heart development |
[102] | Heart tissue (mouse) | Healthy | E14.5, E17.5, NB, P7, P14, adult | The DNA methylation levels of CpG dinucleotides region in ssTnI gene promoter were detected using MSP and BSP | DNA methylation levels of the CpG dinucleotides region in ssTnI gene promoter were increased with the development of mouse heart |
[103] | Heart tissue (mouse) | Healthy | P1, P7, P14, P28, P84 (n = 3 per group) | For analysis of global DNA methylation, 5‐methylcytosine levels were measured using the MethylFlash Methylated DNA Quantification Kit | Majority of DMRs (~ 80%) were hypermethylated between P1 and P14, and hypermethylated regions were associated with transcriptional shut down of important developmental signaling pathway |
[101] | Heart tissue (mouse) | Chronic pressure overload in adult mice | newborn, adult healthy and failing hearts (n = 3–6) | DNA methylome were analyzed by whole-genome bisulfite sequencing | Identified large genomic regions that are differentially methylated during cardiomyocyte development and maturation |