Genomic structural variations for cardiovascular and metabolic comorbidity

The objective of this study was to identify genes targeted by both copy number and copy-neutral changes in the right coronary arteries in the area of advanced atherosclerotic plaques and intact internal mammary arteries derived from the same individuals with comorbid coronary artery disease and meta...

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Bibliographic Details
Published in:Scientific reports 2017-01, Vol.7 (1), p.41268-41268, Article 41268
Main Authors: Nazarenko, Maria S, Sleptcov, Aleksei A, Lebedev, Igor N, Skryabin, Nikolay A, Markov, Anton V, Golubenko, Maria V, Koroleva, Iuliia A, Kazancev, Anton N, Barbarash, Olga L, Puzyrev, Valery P
Format: Article
Language:English
Subjects:
Arteriosclerosis
Cardiovascular disease
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
Comorbidity
Comparative Genomic Hybridization
Copy number
Coronary artery
Coronary Artery Disease - genetics
Coronary vessels
Deoxyribonucleic acid
DNA
DNA Copy Number Variations - genetics
Genomics
Heart diseases
Humans
Hybridization
Male
Metabolic syndrome
Metabolic Syndrome - epidemiology
Metabolic Syndrome - genetics
Metabolism
Middle Aged
Plaques
Real-Time Polymerase Chain Reaction
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Summary:The objective of this study was to identify genes targeted by both copy number and copy-neutral changes in the right coronary arteries in the area of advanced atherosclerotic plaques and intact internal mammary arteries derived from the same individuals with comorbid coronary artery disease and metabolic syndrome. The artery samples from 10 patients were screened for genomic imbalances using array comparative genomic hybridization. Ninety high-confidence, identical copy number variations (CNVs) were detected. We also identified eight copy-neutral changes (cn-LOHs) > 1.5 Mb in paired arterial samples in 4 of 10 individuals. The frequencies of the two gains located in the 10q24.31 (ERLIN1) and 12q24.11 (UNG, ACACB) genomic regions were evaluated in 33 paired arteries and blood samples. Two patients contained the gain in 10q24.31 (ERLIN1) and one patient contained the gain in 12q24.11 (UNG, ACACB) that affected only the blood DNA. An additional two patients harboured these CNVs in both the arteries and blood. In conclusion, we discovered and confirmed a gain of the 10q24.31 (ERLIN1) and 12q24.11 (UNG, ACACB) genomic regions in patients with coronary artery disease and metabolic comorbidity. Analysis of DNA extracted from blood indicated a possible somatic origin for these CNVs.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep41268