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Title: ETOH inhibits embryonic neural stem/precursor cell proliferation via PLD signaling

Abstract

While a mother's excessive alcohol consumption during pregnancy is known to have adverse effects on fetal neural development, little is known about the underlying mechanism of these effects. In order to investigate these mechanisms, we investigated the toxic effect of ethanol (ETOH) on neural stem/precursor cell (NSC) proliferation. In cultures of NSCs, phospholipase D (PLD) is activated following stimulation with epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF2). Exposure of NSCs to ETOH suppresses cell proliferation, while it has no effect on cell death. Phosphatidic acid (PA), which is a signaling messenger produced by PLD, reverses ETOH inhibition of NSC proliferation. Blocking the PLD signal by 1-butanol suppresses the proliferation. ETOH-induced suppression of NSC proliferation and the protective effect of PA for ETOH-induced suppression are mediated through extracellular signal-regulated kinase signaling. These results indicate that exposure to ETOH impairs NSC proliferation by altering the PLD signaling pathway.

Authors:
 [1];  [2];  [1];  [3];  [1];  [1];  [2];  [1]
  1. Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535 (Japan)
  2. (Japan)
  3. Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535 (Japan), E-mail: asanbe@nch.go.jp
Publication Date:
OSTI Identifier:
21143697
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 370; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2008.03.060; PII: S0006-291X(08)00522-6; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BUTANOLS; CELL PROLIFERATION; ETHANOL; FIBROBLASTS; GROWTH FACTORS; INHIBITION; LASER RADIATION; PREGNANCY; PULSED IRRADIATION; STIMULATION; TOXICITY

Citation Formats

Fujita, Yuko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, Hiroyama, Masami, Sanbe, Atsushi, Yamauchi, Junji, Murase, Shoko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, and Tanoue, Akito. ETOH inhibits embryonic neural stem/precursor cell proliferation via PLD signaling. United States: N. p., 2008. Web. doi:10.1016/j.bbrc.2008.03.060.
Fujita, Yuko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, Hiroyama, Masami, Sanbe, Atsushi, Yamauchi, Junji, Murase, Shoko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, & Tanoue, Akito. ETOH inhibits embryonic neural stem/precursor cell proliferation via PLD signaling. United States. doi:10.1016/j.bbrc.2008.03.060.
Fujita, Yuko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, Hiroyama, Masami, Sanbe, Atsushi, Yamauchi, Junji, Murase, Shoko, Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006, and Tanoue, Akito. 2008. "ETOH inhibits embryonic neural stem/precursor cell proliferation via PLD signaling". United States. doi:10.1016/j.bbrc.2008.03.060.
@article{osti_21143697,
title = {ETOH inhibits embryonic neural stem/precursor cell proliferation via PLD signaling},
author = {Fujita, Yuko and Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006 and Hiroyama, Masami and Sanbe, Atsushi and Yamauchi, Junji and Murase, Shoko and Research and Development Division, Biomaster, Inc., 3-35 Minaminakatohri, Naka-ku, Yokohama, Kanagawa 231-0006 and Tanoue, Akito},
abstractNote = {While a mother's excessive alcohol consumption during pregnancy is known to have adverse effects on fetal neural development, little is known about the underlying mechanism of these effects. In order to investigate these mechanisms, we investigated the toxic effect of ethanol (ETOH) on neural stem/precursor cell (NSC) proliferation. In cultures of NSCs, phospholipase D (PLD) is activated following stimulation with epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF2). Exposure of NSCs to ETOH suppresses cell proliferation, while it has no effect on cell death. Phosphatidic acid (PA), which is a signaling messenger produced by PLD, reverses ETOH inhibition of NSC proliferation. Blocking the PLD signal by 1-butanol suppresses the proliferation. ETOH-induced suppression of NSC proliferation and the protective effect of PA for ETOH-induced suppression are mediated through extracellular signal-regulated kinase signaling. These results indicate that exposure to ETOH impairs NSC proliferation by altering the PLD signaling pathway.},
doi = {10.1016/j.bbrc.2008.03.060},
journal = {Biochemical and Biophysical Research Communications},
number = 1,
volume = 370,
place = {United States},
year = 2008,
month = 5
}
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