Promoter DNA methylation regulates murine SUR1 (Abcc8) and SUR2 (Abcc9) expression in HL-1 cardiomyocytes.

PLoS One

Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, F. Edward Hebert School of Medicine, Bethesda, Maryland, United States of America.

Published: November 2012

AI Article Synopsis

  • The study focuses on how two specific mammalian genes (SUR1 and SUR2) combine with Kir6.2 to form KATP channels in heart cells, which have different properties depending on their composition.
  • It was found that SUR1 is much more expressed than SUR2 in these cells, and this difference is linked to high levels of CpG methylation that silences SUR2's expression.
  • Treatment with a DNA demethylating agent, Aza-dC, increases SUR2 expression, but it also affects SUR1, indicating that DNA methylation is not the sole regulator of these genes' expression.

Article Abstract

Two mammalian genes encode the SURx (SUR1, Abcc8 and SUR2, Abcc9) subunits that combine with Kir6.2 (Kcnj11) subunits to form the ATP-sensitive potassium (KATP) channel in cardiac myocytes. Different isoform combinations endow the channel with distinct physiological and pharmacological properties, and we have recently reported that the molecular composition of sarcolemmal KATP channels is chamber specific in the mouse heart. KATP channel composition is determined by what subunits are expressed in a cell or tissue. In the present study, we explore the role of CpG methylation in regulating SUR1 and SUR2 expression. In HL-1 cardiomyocytes, as in atrial myocytes, SUR1 expression is markedly greater than SUR2. Consistent with CpG methylation-dependent silencing of SUR2 expression, bisulfite sequencing of genomic DNA isolated from HL-1 cells demonstrates that 57.6% of the CpGs in the promoter region of the SUR2 gene are methylated, compared with 0.14% of the the CpG residues in the SUR1 sequence. Moreover, treatment with 10 µM 5-aza-2'-deoxycytidine (Aza-dC) significantly increased both the unmethylated fraction of the SUR2 CpG island and mRNA expression. However, we cannot rule out additional mechanisms of Aza-dC action, as Aza-dC also causes a decrease in SUR1 expression and lower doses of Aza-dC do not alter the unmethylated DNA fraction but do elicit a small increase in SUR2 expression. The conclusion that DNA methylation alone is not the only regulator of SUR subunit expression is also consistent with observations in native myocytes, where the CpG islands of both SUR genes are essentially unmethylated in both atrial and ventricular myocytes. Collectively, these data demonstrate the potential for CpG methylation to regulate SURx subunit expression and raises the possibility that regulated or aberrant CpG methylation might play a role in controlling channel structure and function under different physiological conditions or different species.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402388PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0041533PLOS

Publication Analysis

Top Keywords

cpg methylation
12
sur2 expression
12
expression
9
dna methylation
8
sur1 abcc8
8
sur2
8
abcc8 sur2
8
sur2 abcc9
8
expression hl-1
8
hl-1 cardiomyocytes
8

Similar Publications

Background: Glioblastoma is the commonest malignant brain tumor and has a very poor prognosis. Reduced expression of the MGMT gene (10q26.3), influenced primarily by the methylation of two differentially methylated regions (DMR1 and DMR2), is associated with a good response to temozolomide treatment.

View Article and Find Full Text PDF

Resolving the molecular basis of a Mendelian condition remains challenging owing to the diverse mechanisms by which genetic variants cause disease. To address this, we developed a synchronized long-read genome, methylome, epigenome and transcriptome sequencing approach, which enables accurate single-nucleotide, insertion-deletion and structural variant calling and diploid de novo genome assembly. This permits the simultaneous elucidation of haplotype-resolved CpG methylation, chromatin accessibility and full-length transcript information in a single long-read sequencing run.

View Article and Find Full Text PDF

Context-specific eQTLs provide deeper insight into causal genes underlying shared genetic architecture of critically ill COVID-19 and idiopathic pulmonary fibrosis.

HGG Adv

January 2025

Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA; University Program in Genetics and Genomics, Duke University, Durham, NC, USA; Division of Infectious Diseases, Department of Medicine, Duke University School of Medicine, Durham, NC, USA. Electronic address:

Most genetic variants identified through genome-wide association studies (GWAS) are suspected to be regulatory in nature, but only a small fraction colocalize with expression quantitative trait loci (eQTLs, variants associated with expression of a gene). Therefore, it is hypothesized but largely untested that integration of disease GWAS with context-specific eQTLs will reveal the underlying genes driving disease associations. We used colocalization and transcriptomic analyses to identify shared genetic variants and likely causal genes associated with critically ill COVID-19 and idiopathic pulmonary fibrosis.

View Article and Find Full Text PDF

Background: Urothelial carcinoma (UC) is a common malignancy worldwide. Aberrant DNA methylation is implicated in UC carcinogenesis. This study sought to delineate the DNA methylation landscape in UC and identify DNA methylation-based biomarkers for early detection of UC.

View Article and Find Full Text PDF

Association between epigenome-wide DNA methylation changes and early neurodevelopment in preschool children: Evidence from a former impoverished county in Central China.

Gene

January 2025

Department of Maternal and Child Health School of Public Health Tongji Medical College Huazhong University of Science and Technology Wuhan China; Key Laboratory of Environment and Health, Ministry of Education and Ministry of Environmental Protection, State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, Hubei 430030, China. Electronic address:

Background: Existing epigenome-wide association study (EWAS) investigating the association between DNA methylation (DNAm) and child neurodevelopment have been predominantly conducted within Western populations, and yielded inconsistent results, leading to a significant gap within non-Western setting, particularly in resource-limited rural areas of Central China.

Objectives: To investigate the association between altered epigenome-wide DNAm and neurodevelopment in preschool children from resource-limited rural areas of Central China.

Methods: This case-control study involved 64 preschoolers.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!