DNA methylation and expression of KCNQ3 in bipolar disorder
Objectives Accumulating evidence implicates the potassium voltage‐gated channel, KQT‐like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M‐current and an increase in neuronal hyper...
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| Published in | Bipolar disorders Vol. 17; no. 2; pp. 150 - 159 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Denmark
Blackwell Publishing Ltd
01.03.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1398-5647 1399-5618 1399-5618 |
| DOI | 10.1111/bdi.12230 |
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| Abstract | Objectives
Accumulating evidence implicates the potassium voltage‐gated channel, KQT‐like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M‐current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD.
Methods
DNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real‐time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute.
Results
Significantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion.
Conclusion
The results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition‐induced heterogeneity in psychiatric studies of the brain. |
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| AbstractList | Accumulating evidence implicates the potassium voltage-gated channel, KQT-like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M-current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD.
DNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real-time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute.
Significantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion.
The results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition-induced heterogeneity in psychiatric studies of the brain. Accumulating evidence implicates the potassium voltage-gated channel, KQT-like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M-current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD. DNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real-time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute. Significantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion. The results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition-induced heterogeneity in psychiatric studies of the brain. Objectives Accumulating evidence implicates the potassium voltage‐gated channel, KQT‐like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M‐current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD. Methods DNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real‐time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute. Results Significantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion. Conclusion The results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition‐induced heterogeneity in psychiatric studies of the brain. Accumulating evidence implicates the potassium voltage-gated channel, KQT-like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M-current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD.OBJECTIVESAccumulating evidence implicates the potassium voltage-gated channel, KQT-like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar disorder (BPD). Reduced KCNQ2 or KCNQ3 gene expression might lead to a loss of inhibitory M-current and an increase in neuronal hyperexcitability in disease. The goal of the present study was to evaluate epigenetic and gene expression associations of the KCNQ2 and KCNQ3 genes with BPD.DNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real-time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute.METHODSDNA methylation and gene expression levels of alternative transcripts of KCNQ2 and KCNQ3 capable of binding the ankyrin G (ANK3) gene were evaluated using bisulfite pyrosequencing and the quantitative real-time polymerase chain reaction in the postmortem prefrontal cortex of subjects with BPD and matched controls from the McLean Hospital. Replication analyses of DNA methylation findings were performed using prefrontal cortical DNA obtained from the Stanley Medical Research Institute.Significantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion.RESULTSSignificantly lower expression was observed in KCNQ3, but not KCNQ2. DNA methylation analysis of CpGs within an alternative exonic region of KCNQ3 exon 11 demonstrated significantly lower methylation in BPD, and correlated significantly with KCNQ3 mRNA levels. Lower KCNQ3 exon 11 DNA methylation was observed in the Stanley Medical Research Institute replication cohort, although only after correcting for mood stabilizer status. Mood stabilizer treatment in rats resulted in a slight DNA methylation increase at the syntenic KCNQ3 exon 11 region, which subsequent analyses suggested could be the result of alterations in neuronal proportion.The results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition-induced heterogeneity in psychiatric studies of the brain.CONCLUSIONThe results of the present study suggest that epigenetic alterations in the KCNQ3 gene may be important in the etiopathogenesis of BPD and highlight the importance of controlling for medication and cellular composition-induced heterogeneity in psychiatric studies of the brain. |
| Author | Guintivano, Jerry Saleh, Lena Kaminsky, Zachary Zandi, Peter Potash, James B Lee, Richard S Jones, Ilenna Trivedi, Hersh Akman, Ryan Verma, Ranjana |
| Author_xml | – sequence: 1 givenname: Zachary surname: Kaminsky fullname: Kaminsky, Zachary email: Corresponding author:Zachary Kaminsky, Ph.D.Department of Psychiatry and Behavioral SciencesJohns Hopkins University720 Rutland AvenueRoss Research Building 1070Baltimore, MD 21205USAFax: 410-502-0065, zkamins1@jhmi.edu organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 2 givenname: Ilenna surname: Jones fullname: Jones, Ilenna organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 3 givenname: Ranjana surname: Verma fullname: Verma, Ranjana organization: Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, MD, Bethesda, USA – sequence: 4 givenname: Lena surname: Saleh fullname: Saleh, Lena organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 5 givenname: Hersh surname: Trivedi fullname: Trivedi, Hersh organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 6 givenname: Jerry surname: Guintivano fullname: Guintivano, Jerry organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 7 givenname: Ryan surname: Akman fullname: Akman, Ryan organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 8 givenname: Peter surname: Zandi fullname: Zandi, Peter organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD, USA – sequence: 9 givenname: Richard S surname: Lee fullname: Lee, Richard S organization: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, MD, Baltimore, USA – sequence: 10 givenname: James B surname: Potash fullname: Potash, James B organization: Department of Psychiatry, University of Iowa, IA, Iowa City, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25041603$$D View this record in MEDLINE/PubMed |
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| Copyright | 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. |
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| Keywords | bipolar disorder DNA methylation KCNQ3 pyrosequencing glia neurons epigenetics |
| Language | English |
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| Notes | istex:B35F96FAC6BBDD6F475B8A0523DA254E3BA43BB7 Figure S1. DNA methylation at the SP1Motif [specificity protein 1 (SP1)] CpG6 and exon 11 positions versus steady-state mRNA levels of the potassium voltage-gated channel, KQT-like subfamily, member 3 (KCNQ3)-AB transcript are depicted for the Harvard Brain Tissue Resource Center at McLean Hospital (McL) brain tissue (A) and for the neuronal model (B). As SP1 transcription factor and RE1-silencing transcription factor (REST) transcriptional corepressor binding is reported to modulate KCNQ3 expression, we evaluated the relationship of DNA methylation in the context of the gene expression levels of these two factors in the McL cohort. Gene expression data generated on the Affymetrix HGU133A gene expression microarray platform (Gene Expression Omnibus Platform: GPL96) was downloaded for the McL cohort from the National Brain Databank (http://national_databank.mclean.harvard.edu/brainbank/Main) and the gene expression values for the SP1 and REST genes were incorporated into the additive model. All factors displayed significant association in the additive model (SP1 expression β = −21.27 ± 7.19, p = 0.018; REST expression β = 12.44 ± 4.61, p = 0.027; SP1Motif CpG 6 methylation β = 0.52 ± 0.21, p = 0.035; exon 11 methylation β = 1 ± 0.2, p = 0.0009), while the adjusted R2 increased to 0.77 (p = 0.0026). This analysis corroborates the known effect of SP1 and REST transcriptional control on KCNQ3 and highlights that epigenetic modulation at SP1Motif CpG6 and exon 11 remain important when relevant transcription factor expression is controlled for. Table S1. Pyrosequencing primers. Table S2. KCNQ3 exon 11 DNA methylation versus covariates. ArticleID:BDI12230 ark:/67375/WNG-947ZTQSR-3 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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| PublicationTitle | Bipolar disorders |
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Accumulating evidence implicates the potassium voltage‐gated channel, KQT‐like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of... Accumulating evidence implicates the potassium voltage-gated channel, KQT-like subfamily, member 2 and 3 (KCNQ2 and KCNQ3) genes in the etiology of bipolar... |
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| SubjectTerms | Adult Aged Animals Antimanic Agents - pharmacology Base Sequence bipolar disorder Bipolar Disorder - genetics Brain - drug effects Brain - metabolism Case-Control Studies Cell Line, Tumor DNA methylation DNA Methylation - genetics Epigenesis, Genetic epigenetics Female Gene Expression Profiling glia Humans KCNQ2 Potassium Channel - drug effects KCNQ2 Potassium Channel - genetics KCNQ3 KCNQ3 Potassium Channel - drug effects KCNQ3 Potassium Channel - genetics Lithium Compounds - pharmacology Male Middle Aged Molecular Sequence Data neurons Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism pyrosequencing Rats Real-Time Polymerase Chain Reaction RNA, Messenger - drug effects RNA, Messenger - metabolism Valproic Acid - pharmacology |
| Title | DNA methylation and expression of KCNQ3 in bipolar disorder |
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