DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder

Hiroko Sugawara, Yui Murata, Tempei Ikegame, Rie Sawamura, Shota Shimanaga, Yusuke Takeoka, Takeo Saito, Masashi Ikeda, Akane Yoshikawa, Fumichika Nishimura, Yoshiya Kawamura, Chihiro Kakiuchi, Tsukasa Sasaki, Nakao Iwata, Mamoru Hashimoto, Kiyoto Kasai, Tadafumi Kato, Miki Bundo, Kazuya Iwamoto

Research output: Contribution to journalArticle

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Abstract

Aim: Schizophrenia (SZ) and bipolar disorder (BD) have been known to share genetic and environmental risk factors, and complex gene–environmental interactions may contribute to their pathophysiology. In contrast to high genetic overlap between SZ and BD, as revealed by genome-wide association studies, the extent of epigenetic overlap remains largely unknown. In the present study, we explored whether SZ and BD share epigenetic risk factors in the same manner as they share genetic components. Methods: We performed DNA methylation analyses of the CpG sites in the top five candidate regions (FAM63B, ARHGAP26, CTAGE11P, TBC1D22A, and intergenic region [IR] on chromosome 16) reported in a previous methylome-wide association study (MWAS) of SZ, using whole blood samples from subjects with BD and controls. Results: Among the five candidate regions, the CpG sites in FAM63B and IR on chromosome 16 were significantly hypomethylated in the samples from subjects with BD as well as those from subjects with SZ. On the other hand, the CpG sites in TBC1D22A were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ. Conclusion: Hypomethylation of FAM63B and IR on chromosome 16 could be common epigenetic risk factors for SZ and BD. Further comprehensive epigenetic studies for BD, such as MWAS, will uncover the extent of similarity and uniqueness of epigenetic alterations.

Original languageEnglish
Pages (from-to)245-254
Number of pages10
JournalPsychiatry and clinical neurosciences
Volume72
Issue number4
DOIs
Publication statusPublished - 04-2018

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Genetic Association Studies
DNA Methylation
Bipolar Disorder
Epigenomics
Schizophrenia
Chromosomes, Human, Pair 16
Intergenic DNA
Genome-Wide Association Study

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health

Cite this

Sugawara, Hiroko ; Murata, Yui ; Ikegame, Tempei ; Sawamura, Rie ; Shimanaga, Shota ; Takeoka, Yusuke ; Saito, Takeo ; Ikeda, Masashi ; Yoshikawa, Akane ; Nishimura, Fumichika ; Kawamura, Yoshiya ; Kakiuchi, Chihiro ; Sasaki, Tsukasa ; Iwata, Nakao ; Hashimoto, Mamoru ; Kasai, Kiyoto ; Kato, Tadafumi ; Bundo, Miki ; Iwamoto, Kazuya. / DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder. In: Psychiatry and clinical neurosciences. 2018 ; Vol. 72, No. 4. pp. 245-254.
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title = "DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder",
abstract = "Aim: Schizophrenia (SZ) and bipolar disorder (BD) have been known to share genetic and environmental risk factors, and complex gene–environmental interactions may contribute to their pathophysiology. In contrast to high genetic overlap between SZ and BD, as revealed by genome-wide association studies, the extent of epigenetic overlap remains largely unknown. In the present study, we explored whether SZ and BD share epigenetic risk factors in the same manner as they share genetic components. Methods: We performed DNA methylation analyses of the CpG sites in the top five candidate regions (FAM63B, ARHGAP26, CTAGE11P, TBC1D22A, and intergenic region [IR] on chromosome 16) reported in a previous methylome-wide association study (MWAS) of SZ, using whole blood samples from subjects with BD and controls. Results: Among the five candidate regions, the CpG sites in FAM63B and IR on chromosome 16 were significantly hypomethylated in the samples from subjects with BD as well as those from subjects with SZ. On the other hand, the CpG sites in TBC1D22A were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ. Conclusion: Hypomethylation of FAM63B and IR on chromosome 16 could be common epigenetic risk factors for SZ and BD. Further comprehensive epigenetic studies for BD, such as MWAS, will uncover the extent of similarity and uniqueness of epigenetic alterations.",
author = "Hiroko Sugawara and Yui Murata and Tempei Ikegame and Rie Sawamura and Shota Shimanaga and Yusuke Takeoka and Takeo Saito and Masashi Ikeda and Akane Yoshikawa and Fumichika Nishimura and Yoshiya Kawamura and Chihiro Kakiuchi and Tsukasa Sasaki and Nakao Iwata and Mamoru Hashimoto and Kiyoto Kasai and Tadafumi Kato and Miki Bundo and Kazuya Iwamoto",
year = "2018",
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Sugawara, H, Murata, Y, Ikegame, T, Sawamura, R, Shimanaga, S, Takeoka, Y, Saito, T, Ikeda, M, Yoshikawa, A, Nishimura, F, Kawamura, Y, Kakiuchi, C, Sasaki, T, Iwata, N, Hashimoto, M, Kasai, K, Kato, T, Bundo, M & Iwamoto, K 2018, 'DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder', Psychiatry and clinical neurosciences, vol. 72, no. 4, pp. 245-254. https://doi.org/10.1111/pcn.12645

DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder. / Sugawara, Hiroko; Murata, Yui; Ikegame, Tempei; Sawamura, Rie; Shimanaga, Shota; Takeoka, Yusuke; Saito, Takeo; Ikeda, Masashi; Yoshikawa, Akane; Nishimura, Fumichika; Kawamura, Yoshiya; Kakiuchi, Chihiro; Sasaki, Tsukasa; Iwata, Nakao; Hashimoto, Mamoru; Kasai, Kiyoto; Kato, Tadafumi; Bundo, Miki; Iwamoto, Kazuya.

In: Psychiatry and clinical neurosciences, Vol. 72, No. 4, 04.2018, p. 245-254.

Research output: Contribution to journalArticle

TY - JOUR

T1 - DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder

AU - Sugawara, Hiroko

AU - Murata, Yui

AU - Ikegame, Tempei

AU - Sawamura, Rie

AU - Shimanaga, Shota

AU - Takeoka, Yusuke

AU - Saito, Takeo

AU - Ikeda, Masashi

AU - Yoshikawa, Akane

AU - Nishimura, Fumichika

AU - Kawamura, Yoshiya

AU - Kakiuchi, Chihiro

AU - Sasaki, Tsukasa

AU - Iwata, Nakao

AU - Hashimoto, Mamoru

AU - Kasai, Kiyoto

AU - Kato, Tadafumi

AU - Bundo, Miki

AU - Iwamoto, Kazuya

PY - 2018/4

Y1 - 2018/4

N2 - Aim: Schizophrenia (SZ) and bipolar disorder (BD) have been known to share genetic and environmental risk factors, and complex gene–environmental interactions may contribute to their pathophysiology. In contrast to high genetic overlap between SZ and BD, as revealed by genome-wide association studies, the extent of epigenetic overlap remains largely unknown. In the present study, we explored whether SZ and BD share epigenetic risk factors in the same manner as they share genetic components. Methods: We performed DNA methylation analyses of the CpG sites in the top five candidate regions (FAM63B, ARHGAP26, CTAGE11P, TBC1D22A, and intergenic region [IR] on chromosome 16) reported in a previous methylome-wide association study (MWAS) of SZ, using whole blood samples from subjects with BD and controls. Results: Among the five candidate regions, the CpG sites in FAM63B and IR on chromosome 16 were significantly hypomethylated in the samples from subjects with BD as well as those from subjects with SZ. On the other hand, the CpG sites in TBC1D22A were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ. Conclusion: Hypomethylation of FAM63B and IR on chromosome 16 could be common epigenetic risk factors for SZ and BD. Further comprehensive epigenetic studies for BD, such as MWAS, will uncover the extent of similarity and uniqueness of epigenetic alterations.

AB - Aim: Schizophrenia (SZ) and bipolar disorder (BD) have been known to share genetic and environmental risk factors, and complex gene–environmental interactions may contribute to their pathophysiology. In contrast to high genetic overlap between SZ and BD, as revealed by genome-wide association studies, the extent of epigenetic overlap remains largely unknown. In the present study, we explored whether SZ and BD share epigenetic risk factors in the same manner as they share genetic components. Methods: We performed DNA methylation analyses of the CpG sites in the top five candidate regions (FAM63B, ARHGAP26, CTAGE11P, TBC1D22A, and intergenic region [IR] on chromosome 16) reported in a previous methylome-wide association study (MWAS) of SZ, using whole blood samples from subjects with BD and controls. Results: Among the five candidate regions, the CpG sites in FAM63B and IR on chromosome 16 were significantly hypomethylated in the samples from subjects with BD as well as those from subjects with SZ. On the other hand, the CpG sites in TBC1D22A were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ. Conclusion: Hypomethylation of FAM63B and IR on chromosome 16 could be common epigenetic risk factors for SZ and BD. Further comprehensive epigenetic studies for BD, such as MWAS, will uncover the extent of similarity and uniqueness of epigenetic alterations.

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DO - 10.1111/pcn.12645

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