Genome-wide DNA Methylation Profiling of Blood from Monozygotic Twins Discordant for Myocardial Infarction

Köseler, Aylin; Ma, Feiyang; Kılıç, İsmail Doğu; Morselli, Marco; Kilic, Oguz; Pellegrini, Matteo

doi:10.21873/invivo.11782

Cited by 11 publications

(5 citation statements)

References 27 publications

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“…Cao et al reported that ACSM5 was low expressed in renal tissue of rats with chronic glomerulonephritis (CGN), while Qiteng Xiaozhao granules significantly increased the low expression of ACSM5 in the renal tissue of rats with CGN, suggesting that ACSM5 was involved in the occurrence and development of CGN [ 44 ]. Cao et al found that ACSM5 gene was hypermethylated in the peripheral blood of patients with myocardial infarction, and its methylation site and level might be closely related to the occurrence of myocardial infarction [ 45 ]. However, the role of ACSM5 in the HLF has not been reported yet.…”

Section: Discussionmentioning

confidence: 99%

Integrative analysis of genome-wide DNA methylation and single-nucleotide polymorphism identified ACSM5 as a suppressor of lumbar ligamentum flavum hypertrophy

et al. 2021

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Background Hypertrophy of ligamentum flavum (HLF) is a common lumbar degeneration disease (LDD) with typical symptoms of low back pain and limb numbness owing to an abnormal pressure on spinal nerves. Previous studies revealed HLF might be caused by fibrosis, inflammatory, and other bio-pathways. However, a global analysis of HLF is needed severely. Methods A genome-wide DNA methylation and single-nucleotide polymorphism analysis were performed from five LDD patients with HLF and five LDD patients without HLF. Comprehensive integrated analysis was performed using bioinformatics analysis and the validated experiments including Sanger sequencing, methylation-specific PCR, qPCR and ROC analysis. Furthermore, the function of novel genes in ligamentum flavum cells (LFCs) was detected to explore the molecular mechanism in HLF through knock down experiment, overexpression experiment, CCK8 assay, apoptosis assay, and so on. Results We identified 69 SNP genes and 735 661 differentially methylated sites that were enriched in extracellular matrix, inflammatory, and cell proliferation. A comprehensive analysis demonstrated key genes in regulating the development of HLF including ACSM5. Furthermore, the hypermethylation of ACSM5 that was mediated by DNMT1 led to downregulation of ACSM5 expression, promoted the proliferation and fibrosis, and inhibited the apoptosis of LFCs. Conclusion This study revealed that DNMT1/ACSM5 signaling could enhance HLF properties in vitro as a potential therapeutic strategy for HLF.

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Section: Discussionmentioning

confidence: 99%

Integrative analysis of genome-wide DNA methylation and single-nucleotide polymorphism identified ACSM5 as a suppressor of lumbar ligamentum flavum hypertrophy

et al. 2021

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“…These CpGs sites and genes stress the correlation of ion regulation, lipid metabolism, and inflammation in the MI biological mechanisms (Fernández-Sanlés et al, 2021). Thus, the new DNA methylation sequencing technology can identify potential target sites related to the aberrant epigenetic regulation of MI (Koseler et al, 2020). Additionally, the sites stated by two studies (Guarrera et al, 2015;Nakatochi et al, 2017) are candidates for further assessment as underlying MI biomarkers.…”

Section: Dna Methylation and MImentioning

confidence: 97%

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Chen¹,

Liu²,

Ma³

et al. 2021

Front. Genet.

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Myocardial infarction (MI) is a complicated pathology triggered by numerous environmental and genetic factors. Understanding the effect of epigenetic regulation mechanisms on the cardiovascular disease would advance the field and promote prophylactic methods targeting epigenetic mechanisms. Genetic screening guides individualised MI therapies and surveillance. The present review reported the latest development on the epigenetic regulation of MI in terms of DNA methylation, histone modifications, and microRNA-dependent MI mechanisms and the novel therapies based on epigenetics.

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“…Hypomethylation of the IL6 gene promoter is also associated with this nosology [32]. The study of 27-year-old monozygotic male twins discordant for myocardial infarction showed hypomethylation of the LDAH, APOB, ACSM2A, ACSM5, ACSF3, CES1, CES1P1, AFG3L2, ISCU, SEC14L2, MTTP genes in a twin without myocardial infarction (twins have the same work and have no risk factors associated with pathology) [71].…”

Section: Dna Methylation and Ischemic Heart Diseasementioning

confidence: 99%

Role of DNA Methylation in Development of Cardiovascular Diseases, Resulting in a Sudden Cardiac Death (Review)

Иванова¹,

Maksimova²,

Gurazheva³

2022

Sovrem Tehnol Med

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An effective system to diagnose predisposition to development of sudden cardiac death (SCD) is required in order to determine the risk of developing a sudden fatal outcome well in advance of the onset thereof, including in people with asymptomatic cardiovascular disease, as well as to implement early preventive measures that can result in a decrease in the population mortality from cardiovascular diseases. Thus, the search for SCD risk markers becomes a topical issue for modern health care.According to recent studies, epigenetic mechanisms of heredity, and DNA methylation above all, play an important role in development of many diseases. The review provides the results of recent foreign and Russian studies on identification of a link between DNA methylation and development of cardiovascular diseases being the basis for SCD (IHD, cardiomyopathies, heart rhythm disturbances). The major part of the review is dedicated to studying DNA methylation in IHD, which is the most epigenetically explored nosology at the moment. Attention is also paid to studies of the DNA methylation role in development of acute coronary syndrome and myocardial infarction, which have development mechanisms similar to those of SCD. There were only few studies on identification of a link between DNA methylation and cardiomyopathies and cardiac arrhythmias conducted, however, an association of specific genes methylation with the explored nosologies was revealed. The review also provides pathogenetic substantiations of the possibilities to use epigenetic markers of cardiovascular diseases as SCD markers.Thus, it has been established that study of genes the methylation of which is associated with IHD (CTH, PLCB1, PTX3, MMP9, FN1, F2RL3, ABCB1, FOXP3, GDF15, IL6, CASR), with lipid metabolism disorders and atherosclerosis (CETP, CCL2, SREBF2, TIMP1), as well as with heart rhythm disturbances (SCN5A and KCNQ1), may be most promising in relation to SCD.

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Genome-wide DNA Methylation Profiling of Blood from Monozygotic Twins Discordant for Myocardial Infarction

Cited by 11 publications

References 27 publications

Integrative analysis of genome-wide DNA methylation and single-nucleotide polymorphism identified ACSM5 as a suppressor of lumbar ligamentum flavum hypertrophy

Integrative analysis of genome-wide DNA methylation and single-nucleotide polymorphism identified ACSM5 as a suppressor of lumbar ligamentum flavum hypertrophy

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics

Role of DNA Methylation in Development of Cardiovascular Diseases, Resulting in a Sudden Cardiac Death (Review)

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