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

Identifieur interne : 000000 ( Main/Exploration ); suivant : 000001

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

Auteurs : Aylin Koseler [Turquie] ; Feiyang Ma [États-Unis] ; Ismail Dogu Kilic [Turquie] ; Marco Morselli [États-Unis] ; Oguz Kilic [Turquie] ; Matteo Pellegrini [États-Unis]

Source :

RBID : pubmed:31882500

Descripteurs français

English descriptors

Abstract

BACKGROUND/AIM

This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy.

PATIENTS AND METHODS

Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis.

RESULTS

According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acyl-CoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds.

CONCLUSION

This twin study may contribute significantly to the understanding of the genetic basis of CVD and resulting myocardial infarction. This approach may allow identification of possible target loci associated with aberrant epigenetic regulation in CVD.


DOI: 10.21873/invivo.11782
PubMed: 31882500
PubMed Central: PMC6984093


Affiliations:


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Le document en format XML

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<term>Adult (MeSH)</term>
<term>DNA Methylation (MeSH)</term>
<term>Epigenesis, Genetic (MeSH)</term>
<term>Gene Expression Profiling (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Genetic Markers (MeSH)</term>
<term>Genome, Human (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Myocardial Infarction (blood)</term>
<term>Myocardial Infarction (genetics)</term>
<term>Phenotype (MeSH)</term>
<term>Prognosis (MeSH)</term>
<term>Promoter Regions, Genetic (MeSH)</term>
<term>Twins, Monozygotic (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Adulte (MeSH)</term>
<term>Analyse de profil d'expression de gènes (MeSH)</term>
<term>Génome humain (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Infarctus du myocarde (génétique)</term>
<term>Infarctus du myocarde (sang)</term>
<term>Jumeaux monozygotes (génétique)</term>
<term>Marqueurs génétiques (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Méthylation de l'ADN (MeSH)</term>
<term>Phénotype (MeSH)</term>
<term>Pronostic (MeSH)</term>
<term>Régions promotrices (génétique) (MeSH)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Épigenèse génétique (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en">
<term>Genetic Markers</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en">
<term>Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Myocardial Infarction</term>
<term>Twins, Monozygotic</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Infarctus du myocarde</term>
<term>Jumeaux monozygotes</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr">
<term>Infarctus du myocarde</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>DNA Methylation</term>
<term>Epigenesis, Genetic</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Genome, Human</term>
<term>Humans</term>
<term>Male</term>
<term>Phenotype</term>
<term>Prognosis</term>
<term>Promoter Regions, Genetic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Adulte</term>
<term>Analyse de profil d'expression de gènes</term>
<term>Génome humain</term>
<term>Humains</term>
<term>Marqueurs génétiques</term>
<term>Mâle</term>
<term>Méthylation de l'ADN</term>
<term>Phénotype</term>
<term>Pronostic</term>
<term>Régions promotrices (génétique)</term>
<term>Régulation de l'expression des gènes</term>
<term>Épigenèse génétique</term>
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<front>
<div type="abstract" xml:lang="en">
<p>
<b>BACKGROUND/AIM</b>
</p>
<p>This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>PATIENTS AND METHODS</b>
</p>
<p>Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>RESULTS</b>
</p>
<p>According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acyl-CoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds.</p>
</div>
<div type="abstract" xml:lang="en">
<p>
<b>CONCLUSION</b>
</p>
<p>This twin study may contribute significantly to the understanding of the genetic basis of CVD and resulting myocardial infarction. This approach may allow identification of possible target loci associated with aberrant epigenetic regulation in CVD.</p>
</div>
</front>
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<AbstractText Label="BACKGROUND/AIM" NlmCategory="OBJECTIVE">This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy.</AbstractText>
<AbstractText Label="PATIENTS AND METHODS" NlmCategory="METHODS">Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acyl-CoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds.</AbstractText>
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