Cyclooxygenase-2 is involved in increased proliferation of neuronal progenitor cells in the ischemic mouse hippocampus

Tsutomu Sasaki; Kazuo Kitagawa; Shiro Sugiura; Emi Omura-Matsuoka; Shigeru Tanaka; Yoshiki Yagita; Hideyuki Okano; Masayasu Matsumoto; Masatsugu Hori

doi:10.1016/S0531-5131(03)00071-2

Cyclooxygenase-2 is involved in increased proliferation of neuronal progenitor cells in the ischemic mouse hippocampus

Tsutomu Sasaki, Kazuo Kitagawa, Shiro Sugiura, Emi Omura-Matsuoka, Shigeru Tanaka, Yoshiki Yagita, Hideyuki Okano, Masayasu Matsumoto, Masatsugu Hori

Department of Physiology

Research output: Contribution to journal › Article › peer-review

Abstract

Global ischemia promotes neurogenesis in the dentate gyrus of the adult mouse hippocampus. Cyclooxygenase (COX)-2, the principal isoenzyme in the brain, modulates inflammation, glutamate-mediated cytotoxicity, and synaptic plasticity. The enhancement of dentate gyrus neurogenesis following ischemia was attenuated by COX inhibitors and in COX-2 knockout mice. These results demonstrate that COX-2 may modulate the enhancement of neurogenesis following ischemia.

Original language	English
Pages (from-to)	445-450
Number of pages	6
Journal	International Congress Series
Volume	1252
Issue number	C
DOIs	https://doi.org/10.1016/S0531-5131(03)00071-2
Publication status	Published - 2003 Jun 1

Keywords

COX-2
Hippocampus
Musashi-1
Neurogenesis
Neuronal progenitor

ASJC Scopus subject areas

Medicine(all)

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10.1016/S0531-5131(03)00071-2

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title = "Cyclooxygenase-2 is involved in increased proliferation of neuronal progenitor cells in the ischemic mouse hippocampus",

abstract = "Global ischemia promotes neurogenesis in the dentate gyrus of the adult mouse hippocampus. Cyclooxygenase (COX)-2, the principal isoenzyme in the brain, modulates inflammation, glutamate-mediated cytotoxicity, and synaptic plasticity. The enhancement of dentate gyrus neurogenesis following ischemia was attenuated by COX inhibitors and in COX-2 knockout mice. These results demonstrate that COX-2 may modulate the enhancement of neurogenesis following ischemia.",

keywords = "COX-2, Hippocampus, Musashi-1, Neurogenesis, Neuronal progenitor",

author = "Tsutomu Sasaki and Kazuo Kitagawa and Shiro Sugiura and Emi Omura-Matsuoka and Shigeru Tanaka and Yoshiki Yagita and Hideyuki Okano and Masayasu Matsumoto and Masatsugu Hori",

year = "2003",

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doi = "10.1016/S0531-5131(03)00071-2",

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T1 - Cyclooxygenase-2 is involved in increased proliferation of neuronal progenitor cells in the ischemic mouse hippocampus

AU - Sasaki, Tsutomu

AU - Kitagawa, Kazuo

AU - Sugiura, Shiro

AU - Omura-Matsuoka, Emi

AU - Tanaka, Shigeru

AU - Yagita, Yoshiki

AU - Okano, Hideyuki

AU - Matsumoto, Masayasu

AU - Hori, Masatsugu

PY - 2003/6/1

Y1 - 2003/6/1

N2 - Global ischemia promotes neurogenesis in the dentate gyrus of the adult mouse hippocampus. Cyclooxygenase (COX)-2, the principal isoenzyme in the brain, modulates inflammation, glutamate-mediated cytotoxicity, and synaptic plasticity. The enhancement of dentate gyrus neurogenesis following ischemia was attenuated by COX inhibitors and in COX-2 knockout mice. These results demonstrate that COX-2 may modulate the enhancement of neurogenesis following ischemia.

AB - Global ischemia promotes neurogenesis in the dentate gyrus of the adult mouse hippocampus. Cyclooxygenase (COX)-2, the principal isoenzyme in the brain, modulates inflammation, glutamate-mediated cytotoxicity, and synaptic plasticity. The enhancement of dentate gyrus neurogenesis following ischemia was attenuated by COX inhibitors and in COX-2 knockout mice. These results demonstrate that COX-2 may modulate the enhancement of neurogenesis following ischemia.

KW - COX-2

KW - Hippocampus

KW - Musashi-1

KW - Neurogenesis

KW - Neuronal progenitor

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VL - 1252

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JO - International Congress Series

JF - International Congress Series

IS - C

ER -

Cyclooxygenase-2 is involved in increased proliferation of neuronal progenitor cells in the ischemic mouse hippocampus

Abstract

Keywords

ASJC Scopus subject areas

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