Effects of ubiquitin gene silencing in anoxia-reoxygenation of cultured cardiomyocytes

Vo, Kyrychenko; Nahibin, VS; Lv, Tumanovs'ka; VIe, Dosenko; Vk, Rybal'chenko; Oo, Moĭbenko

doi:10.15407/fz56.04.037

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…2; Table II). This was exemplified by the hypomethylation of anoxia-reoxygenation associated genes in cardiac myocytes including proteasome subunit β 9 (Table II) (24), and human major histocompatibility complex (MHC) family members G, C, DMB, DRB1 and MHC-related protein 1 (20). The large-scale DNA hypomethylation detected in pAF-associated genes were associated with biological processes including sodium and potassium ion transport, cell differentiation, apoptosis and response to oxidation (Table II).…”

Section: Biological Function Analysis Of Differentially Methylated Gementioning

confidence: 99%

Genome-wide DNA methylation analysis in permanent atrial fibrillation

Zhao

Zhou

Gao

et al. 2017

Molecular Medicine Reports

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Atrial fibrillation (AF) is a highly heterogeneous genetic disease; however, the pathogenesis of AF cannot be explained by genetic variants alone. DNA methylation is a heritable method of gene expression regulation, and may be a potential regulatory mechanism in AF. Therefore, in the present study, the genome‑wide DNA methylation pattern in cells derived from the left atrium of patients with permanent AF (n=7) was compared with that of healthy heart donors (n=4) with a normal sinus rhythm (SR). Enriched biological functions of the differentially methylated genes were assessed. Integrated analysis of genome‑wide methylation and mRNA expression profiles was performed, and reverse transcription quantitative‑polymerase chain reaction (RT‑qPCR) was used to determine the expression levels of four selected genes. A total of 417 differentially methylated CpG sites were identified in the fibrillating atrium (P<0.05; |β|>0.17); the majority of which were located in gene‑body and intergenic regions outside of CpG islands. Aberrantly methylated genes participated in the activation of inflammation, sodium and potassium ion transport, fibrosis and the reduction of lipid metabolism. Hypermethylation in the AF susceptible loci, paired‑like homeodomain transcription factor 2 (chromosome 4q25) and coiled‑coil domain containing 141 (chromosome 2q31), as well as hypomethylation in the calcium voltage‑gated channel subunit α1C (chromosome 12p13) locus, were identified in all patients with AF. Of the 420 upregulated and 567 downregulated genes previously identified in patients with AF relative to those with normal SR (fold‑change >2.0; P≤0.05), 12 genes were hypomethylated and eight genes were hypermethylated in each group, respectively (|β|>0.2: P<0.05). RT‑qPCR analysis of four of these genes supported the modulatory effect of DNA methylation on gene expression. These results suggest that DNA methylation‑mediated regulation of gene expression may serve an important role in AF pathogenesis, and several susceptible AF CpG loci were identified which may be involved in the initiation of AF.

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Section: Biological Function Analysis Of Differentially Methylated Gementioning

confidence: 99%

Genome-wide DNA methylation analysis in permanent atrial fibrillation

Zhao

Zhou

Gao

et al. 2017

Molecular Medicine Reports

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“…According to the processed information on the breed structure of dogs with diarrhea, it was found that the emphasis shifted towards small breeds: Spitzes -18.3%, Cocker Spaniels -13%, Yorkies -28.4%, Chihuahuas -12.6%, Totherriers -16.4%, Jack Russell -12.8%. Among the large breeds, Labradors were more likely to be ill -5.2%, German Shepherds, Rottweilers, Dobermans, Bull Terriers, Collie, Bulldogs, Irish Setters, Great Danes, and Dalmatians were less likely to need help -they accounted for 3.7% of the total [2]. This can be explained by the decline in the population of such breeds in urban areas [4].…”

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confidence: 99%