Marked increases in hippocampal neuron indoleamine 2, 3-dioxygenase via IFN-γ-independent pathway following transient global ischemia in mouse

Masato Hoshi, Kuniaki Saito, Yuki Murakami, Ayako Taguchi, Hidetsugu Fujigaki, Ryo Tanaka, Masao Takemura, Hiroyasu Ito, Akira Hara, Mitsuru Seishima

Research output: Contribution to journalArticle

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Abstract

Indoleamine 2, 3-dioxygenase (IDO), which catabolizes L-tryptophan (L-TRP) to L-kynurenine (L-KYN), is an immunoregulatory factor that is up-regulated via an interferon-gamma (IFN-γ)-dependent and/or -independent mechanism. In this study, we investigated the localization of IDO and whether induction of IDO expression is an IFN-γ-dependent and/or -independent mechanism in the CNS after cerebral ischemia. The expressions of IDO protein and mRNA were investigated at different time points following cerebral ischemia using immunohistochemistry, immunofluorescence and RT-PCR. Hippocampal neuron IDO mRNA and immunohistochemical staining were significantly up-regulated 72 h after transient global ischemia. Although IFN-γ is a dominant inducer of IDO, hippocampal neuron IDO was clearly up-regulated in IFN-γ KO mice. In summary, this is the first finding that up-regulation of IDO in hippocampal neurons after transient global ischemia occurs via INF-γ-independent mechanisms.

Original languageEnglish
Pages (from-to)194-198
Number of pages5
JournalNeuroscience Research
Volume63
Issue number3
DOIs
Publication statusPublished - 01-03-2009

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Indoleamine-Pyrrole 2,3,-Dioxygenase
Interferon-gamma
Ischemia
Neurons
Brain Ischemia
Kynurenine
Messenger RNA
Tryptophan
Fluorescent Antibody Technique
Up-Regulation
Immunohistochemistry
Staining and Labeling
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Hoshi, Masato ; Saito, Kuniaki ; Murakami, Yuki ; Taguchi, Ayako ; Fujigaki, Hidetsugu ; Tanaka, Ryo ; Takemura, Masao ; Ito, Hiroyasu ; Hara, Akira ; Seishima, Mitsuru. / Marked increases in hippocampal neuron indoleamine 2, 3-dioxygenase via IFN-γ-independent pathway following transient global ischemia in mouse. In: Neuroscience Research. 2009 ; Vol. 63, No. 3. pp. 194-198.
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Marked increases in hippocampal neuron indoleamine 2, 3-dioxygenase via IFN-γ-independent pathway following transient global ischemia in mouse. / Hoshi, Masato; Saito, Kuniaki; Murakami, Yuki; Taguchi, Ayako; Fujigaki, Hidetsugu; Tanaka, Ryo; Takemura, Masao; Ito, Hiroyasu; Hara, Akira; Seishima, Mitsuru.

In: Neuroscience Research, Vol. 63, No. 3, 01.03.2009, p. 194-198.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Hoshi, Masato

AU - Saito, Kuniaki

AU - Murakami, Yuki

AU - Taguchi, Ayako

AU - Fujigaki, Hidetsugu

AU - Tanaka, Ryo

AU - Takemura, Masao

AU - Ito, Hiroyasu

AU - Hara, Akira

AU - Seishima, Mitsuru

PY - 2009/3/1

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N2 - Indoleamine 2, 3-dioxygenase (IDO), which catabolizes L-tryptophan (L-TRP) to L-kynurenine (L-KYN), is an immunoregulatory factor that is up-regulated via an interferon-gamma (IFN-γ)-dependent and/or -independent mechanism. In this study, we investigated the localization of IDO and whether induction of IDO expression is an IFN-γ-dependent and/or -independent mechanism in the CNS after cerebral ischemia. The expressions of IDO protein and mRNA were investigated at different time points following cerebral ischemia using immunohistochemistry, immunofluorescence and RT-PCR. Hippocampal neuron IDO mRNA and immunohistochemical staining were significantly up-regulated 72 h after transient global ischemia. Although IFN-γ is a dominant inducer of IDO, hippocampal neuron IDO was clearly up-regulated in IFN-γ KO mice. In summary, this is the first finding that up-regulation of IDO in hippocampal neurons after transient global ischemia occurs via INF-γ-independent mechanisms.

AB - Indoleamine 2, 3-dioxygenase (IDO), which catabolizes L-tryptophan (L-TRP) to L-kynurenine (L-KYN), is an immunoregulatory factor that is up-regulated via an interferon-gamma (IFN-γ)-dependent and/or -independent mechanism. In this study, we investigated the localization of IDO and whether induction of IDO expression is an IFN-γ-dependent and/or -independent mechanism in the CNS after cerebral ischemia. The expressions of IDO protein and mRNA were investigated at different time points following cerebral ischemia using immunohistochemistry, immunofluorescence and RT-PCR. Hippocampal neuron IDO mRNA and immunohistochemical staining were significantly up-regulated 72 h after transient global ischemia. Although IFN-γ is a dominant inducer of IDO, hippocampal neuron IDO was clearly up-regulated in IFN-γ KO mice. In summary, this is the first finding that up-regulation of IDO in hippocampal neurons after transient global ischemia occurs via INF-γ-independent mechanisms.

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