Differential genetic associations and expression of PAPST1/SLC35B2 in bipolar disorder and schizophrenia.


Journal

Journal of neural transmission (Vienna, Austria : 1996)
ISSN: 1435-1463
Titre abrégé: J Neural Transm (Vienna)
Pays: Austria
ID NLM: 9702341

Informations de publication

Date de publication:
07 2022
Historique:
received: 23 09 2021
accepted: 12 04 2022
pubmed: 3 5 2022
medline: 25 6 2022
entrez: 2 5 2022
Statut: ppublish

Résumé

Lithium's inhibitory effect on enzymes involved in sulfation process, such as inhibition of 3'(2')-phosphoadenosine 5'-phosphate (PAP) phosphatase, is a possible mechanism of its therapeutic effect for bipolar disorder (BD). 3'-Phosphoadenosine 5'-phosphosulfate (PAPS) is translocated from cytosol to Golgi lumen by PAPS transporter 1 (PAPST1/SLC35B2), where it acts as a sulfa donor. Since SLC35B2 was previously recognized as a molecule that facilitates the release of D-serine, a co-agonist of N-methyl-D-aspartate type glutamate receptor, altered function of SLC35B2 might be associated with the pathophysiology of BD and schizophrenia (SCZ). We performed genetic association analyses of the SLC35B2 gene using Japanese cohorts with 366 BD cases and 370 controls and 2012 SCZ cases and 2170 controls. We then investigated expression of SLC35B2 mRNA in postmortem brains by QPCR using a Caucasian cohort with 33 BD and 34 SCZ cases and 34 controls and by in situ hybridization using a Caucasian cohort with 37 SCZ and 29 controls. We found significant associations between three SNPs (rs575034, rs1875324, and rs3832441) and BD, and significantly reduced SLC35B2 mRNA expression in postmortem dorsolateral prefrontal cortex (DLPFC) of BD. Moreover, we observed normalized SLC35B2 mRNA expression in BD subgroups who were medicated with lithium. While there was a significant association of SLC35B2 with SCZ (SNP rs2233437), its expression was not changed in SCZ. These findings indicate that SLC35B2 might be differentially involved in the pathophysiology of BD and SCZ by influencing the sulfation process and/or glutamate system in the central nervous system.

Identifiants

pubmed: 35501530
doi: 10.1007/s00702-022-02503-7
pii: 10.1007/s00702-022-02503-7
doi:

Substances chimiques

RNA, Messenger 0
SLC35B2 protein, human 0
Sulfate Transporters 0
Lithium 9FN79X2M3F

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

913-924

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.

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Auteurs

Akihito Uezato (A)

School of Health and Welfare, International University of Health and Welfare, Tochigi, Japan.
Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

Daisuke Jitoku (D)

Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

Dai Shimazu (D)

Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Musashishinjo-Kokorono Clinic, Kanagawa, Japan.

Naoki Yamamoto (N)

Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Center for Basic Medical Research, and School of Pharmaceutical Sciences, International University of Health and Welfare, Tochigi, Japan.

Akeo Kurumaji (A)

Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Shimousa-Nakayama Mental Clinic, Chiba, Japan.

Yoshimi Iwayama (Y)

Laboratory for Molecular Psychiatry, RIKEN Center for Brain Science, Saitama, Japan.
Laboratory for Bioinformatics Research, RIKEN Center for Biosystems Dynamics Research, Hyogo, Japan.

Tomoko Toyota (T)

Laboratory for Molecular Psychiatry, RIKEN Center for Brain Science, Saitama, Japan.
Laboratory for Molecular Pathology of Psychiatric Disorders, RIKEN Center for Brain Science, Saitama, Japan.

Takeo Yoshikawa (T)

Laboratory for Molecular Psychiatry, RIKEN Center for Brain Science, Saitama, Japan.
Office of the Center Director, RIKEN Center for Brain Science, Saitama, Japan.

Vahram Haroutunian (V)

Department of Psychiatry and Neuroscience, The Icahn School of Medicine at Mount Sinai, Bronx, NY, USA.

Eduard Bentea (E)

Neurosciences TA Biology, UCB BioPharma SPRL, Braine-l'Alleud, Belgium.

Jarek Meller (J)

Departments of Environmental Health, Electrical Engineering and Computing Systems and Biomedical Informatics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.

Courtney R Sullivan (CR)

Cyagen US Inc., Santa Clara, CA, USA.

James H Meador-Woodruff (JH)

Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Alabama, USA.

Robert E McCullumsmith (RE)

Department of Neuroscience, University of Toledo, Toledo, OH, USA.
Promedica, Toledo, OH, USA.

Toru Nishikawa (T)

Department of Psychiatry and Behavioral Sciences, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan. torunishi@med.showa-u.ac.jp.
Department of Pharmacology, Faculty of Medicine, and Pharmacological Research Center, Showa University, 1-5-8, Shinagawa-ku, Tokyo, 142-8555, Japan. torunishi@med.showa-u.ac.jp.

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