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Title: Expression analysis for inverted effects of serotonin transporter inactivation

Abstract

Inactivation of serotonin transporter (HTT) by pharmacologically in the neonate or genetically increases risk for depression in adulthood, whereas pharmacological inhibition of HTT ameliorates symptoms in depressed patients. The differing role of HTT function during early development and in adult brain plasticity in causing or reversing depression remains an unexplained paradox. To address this we profiled the gene expression of adult Htt knockout (Htt KO) mice and HTT inhibitor-treated mice. Inverted profile changes between the two experimental conditions were seen in 30 genes. Consistent results of the upstream regulatory element search and the co-localization search of these genes indicated that the regulation may be executed by Pax5, Pax7 and Gata3, known to be involved in the survival, proliferation, and migration of serotonergic neurons in the developing brain, and these factors are supposed to keep functioning to regulate downstream genes related to serotonin system in the adult brain.

Authors:
 [1];  [1]; ;  [1];  [2];  [2];  [2];  [3];  [4]
  1. Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045 (Japan)
  2. Computational Biomechanics Unit, Discovery Research Institute, RIKEN, 2-1 Hirosawa Wako City, Saitama 351-0198 (Japan)
  3. Molecular and Clinical Psychobiology, Department of Psychiatry and Psychotherapy, Univ. of Wuerzburg Fuechsleinstr. 15, 97080 Wuerzburg (Germany)
  4. Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), RIKEN Yokohama Inst., 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045 (Japan)
Publication Date:
OSTI Identifier:
21043670
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 368; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2008.01.041; PII: S0006-291X(08)00062-4; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BRAIN; CELL PROLIFERATION; GENE REGULATION; GENES; KNOCK-OUT REACTIONS; MICE; NEONATES; NERVE CELLS; SEROTONIN

Citation Formats

Ichikawa, Manabu, Division of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City University, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Okamura-Oho, Yuko, Shimokawa, Kazuro, Kondo, Shinji, Nakamura, Sakiko, Yokota, Hideo, Bio-research Infrastructure Construction Team, V-CAD System Research, Program, Center for Intellectual Property Strategies, RIKEN, 2-1 Hirosawa Wako City, Saitama 351-0198, Himeno, Ryutaro, Lesch, Klaus-Peter, Hayashizaki, Yoshihide, and Div. of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City Univ., 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045. Expression analysis for inverted effects of serotonin transporter inactivation. United States: N. p., 2008. Web. doi:10.1016/j.bbrc.2008.01.041.
Ichikawa, Manabu, Division of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City University, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Okamura-Oho, Yuko, Shimokawa, Kazuro, Kondo, Shinji, Nakamura, Sakiko, Yokota, Hideo, Bio-research Infrastructure Construction Team, V-CAD System Research, Program, Center for Intellectual Property Strategies, RIKEN, 2-1 Hirosawa Wako City, Saitama 351-0198, Himeno, Ryutaro, Lesch, Klaus-Peter, Hayashizaki, Yoshihide, & Div. of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City Univ., 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045. Expression analysis for inverted effects of serotonin transporter inactivation. United States. https://doi.org/10.1016/j.bbrc.2008.01.041
Ichikawa, Manabu, Division of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City University, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Okamura-Oho, Yuko, Shimokawa, Kazuro, Kondo, Shinji, Nakamura, Sakiko, Yokota, Hideo, Bio-research Infrastructure Construction Team, V-CAD System Research, Program, Center for Intellectual Property Strategies, RIKEN, 2-1 Hirosawa Wako City, Saitama 351-0198, Himeno, Ryutaro, Lesch, Klaus-Peter, Hayashizaki, Yoshihide, and Div. of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City Univ., 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045. 2008. "Expression analysis for inverted effects of serotonin transporter inactivation". United States. https://doi.org/10.1016/j.bbrc.2008.01.041.
@article{osti_21043670,
title = {Expression analysis for inverted effects of serotonin transporter inactivation},
author = {Ichikawa, Manabu and Division of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City University, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045 and Okamura-Oho, Yuko and Shimokawa, Kazuro and Kondo, Shinji and Nakamura, Sakiko and Yokota, Hideo and Bio-research Infrastructure Construction Team, V-CAD System Research, Program, Center for Intellectual Property Strategies, RIKEN, 2-1 Hirosawa Wako City, Saitama 351-0198 and Himeno, Ryutaro and Lesch, Klaus-Peter and Hayashizaki, Yoshihide and Div. of Genomic Information Resources, Science of Biological Supramolecular Systems, Graduate School of Integrated Science, Yokohama City Univ., 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045},
abstractNote = {Inactivation of serotonin transporter (HTT) by pharmacologically in the neonate or genetically increases risk for depression in adulthood, whereas pharmacological inhibition of HTT ameliorates symptoms in depressed patients. The differing role of HTT function during early development and in adult brain plasticity in causing or reversing depression remains an unexplained paradox. To address this we profiled the gene expression of adult Htt knockout (Htt KO) mice and HTT inhibitor-treated mice. Inverted profile changes between the two experimental conditions were seen in 30 genes. Consistent results of the upstream regulatory element search and the co-localization search of these genes indicated that the regulation may be executed by Pax5, Pax7 and Gata3, known to be involved in the survival, proliferation, and migration of serotonergic neurons in the developing brain, and these factors are supposed to keep functioning to regulate downstream genes related to serotonin system in the adult brain.},
doi = {10.1016/j.bbrc.2008.01.041},
url = {https://www.osti.gov/biblio/21043670}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 368,
place = {United States},
year = {Fri Mar 28 00:00:00 EDT 2008},
month = {Fri Mar 28 00:00:00 EDT 2008}
}