MIZUO Keisuke

写真a

Affiliation

School of Medicine, Department of Legal Medicine

Job title

Lecturer
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Research Experience 【 display / non-display 】

  • 2008.04
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    Now

    札幌医科大学   助教・医学部

    助教・医学部

  • 2007.04
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    2008.03

    東京理科大学総合研究機構   ポストドクトラル研究員

    ポストドクトラル研究員

  • 2004.04
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    2007.03

    Temple University School of Medicine   Postdoctoral fellow

    Postdoctoral fellow

  • 2004.03
    　
    　

    星薬科大学大学院薬学研究科博士課程後期修了   博士 (薬学) 取得

    博士 (薬学) 取得

  • 2001.04
    -
    2004.03

    星薬科大学大学院薬学研究科博士課程後期   大学院生

    大学院生

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Professional Memberships 【 display / non-display 】

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    International Society for Biomedical Research on Alcoholism

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    日本法医学会

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    日本神経科学学会

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    日本アルコール・薬物医学会

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    Society for Neuroscience

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Research Areas 【 display / non-display 】

  • Life sciences   Pharmaceuticals - health and biochemistry  

  • Life sciences   Forensic medicine  

  • Life sciences   Pharmacology  

  • Life sciences   Neuroscience - general  

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Research Interests 【 display / non-display 】

  • アルコール

  • 薬物依存

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Papers 【 display / non-display 】

  • Maternal exposure to nanoparticulate titanium dioxide during the prenatal period alters gene expression related to brain development in the mouse

    Midori Shimizu, Hitoshi Tainaka, Taro Oba, Keisuke Mizuo, Masakazu Umezawa, Ken Takeda

    PARTICLE AND FIBRE TOXICOLOGY ( BIOMED CENTRAL LTD )  6   20  2009.07  [Refereed]

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    Background: Nanotechnology is developing rapidly throughout the world and the production of novel man-made nanoparticles is increasing, it is therefore of concern that nanomaterials have the potential to affect human health. The purpose of this study was to investigate the effects of maternal exposure to nano-sized anatase titanium dioxide (TiO2) on gene expression in the brain during the developmental period using cDNA microarray analysis combined with Gene Ontology (GO) and Medical Subject Headings (MeSH) terms information. Results: Analysis of gene expression using GO terms indicated that expression levels of genes associated with apoptosis were altered in the brain of newborn pups, and those associated with brain development were altered in early age. The genes associated with response to oxidative stress were changed in the brains of 2 and 3 weeks old mice. Changes of the expression of genes associated with neurotransmitters and psychiatric diseases were found using MeSH terms. Conclusion: Maternal exposure of mice to TiO2 nanoparticles may affect the expression of genes related to the development and function of the central nervous system.

    DOI PubMed

  • Effect of prenatal exposure to diesel exhaust on dopaminergic system in mice

    Satoshi Yokota, Keisuke Mizuo, Nozomu Moriya, Shigeru Oshio, Isamu Sugawara, Ken Takeda

    NEUROSCIENCE LETTERS ( ELSEVIER IRELAND LTD )  449 ( 1 ) 38 - 41  2009.01  [Refereed]

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    Diesel exhaust (DE) is composed of particles and gaseous compounds. It has been reported that DE causes pulmonary and cardiovascular disease. We have previously reported that fetal exposure to DE had deleterious effects to the reproductive system of mice offspring. However, there is still little known about the effects of prenatal exposure to DE to the central nervous system (CNS). In the present study, we found that prenatal exposure to DE induced reduction of locomotion, furthermore, dopamine (DA) turnover was significantly decreased in the striatum and nucleus accumbens. These results suggest that prenatal exposure to DE has an effect on the CNS. Hypolocomotion could be due to a decrease in DA turnover associated with DA nervous system abnormality. The present study provides the possibility that maternally inhaled DE might influence the development of central dopaminergic system and result in behavior disorder. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

    DOI PubMed

  • Changes in central dopaminergic systems and morphine reward by prenatal and neonatal exposure to bisphenol-A in mice: evidence for the importance of exposure period

    Minoru Narita, Kazuya Miyagawa, Keisuke Mizuo, Takuya Yoshida, Tsutomu Suzuki

    ADDICTION BIOLOGY ( BLACKWELL PUBLISHING )  12 ( 2 ) 167 - 172  2007.06  [Refereed]

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    Bisphenol-A has been extensively evaluated for toxicity in a variety of tests as the most common environmental endocrine disruptors. In a previous study, we reported that exposure to bisphenol-A affects the development of the central dopaminergic system in the mouse limbic area. The present study was undertaken to investigate the relationship between the developmental toxicity of bisphenol-A and its exposure period. The exposure to bisphenol-A during either organogenesis or lactation, but not implantation and parturition, significantly enhanced the morphine-induced hyperlocomotion and rewarding effects. Furthermore, exposure to bisphenol-A during either organogenesis or lactation also produced an up-regulation of dopamine receptor function to activate G-protein in the mouse limbic forebrain. These results indicate that both organogenesis and lactation are more sensitive to the bisphenol-A-induced developmental neuronal toxicology than any other periods. In conclusion, the present data suggest that the organogenesis and lactation are the most important period to cause the alternation of dopaminergic system by bisphenol-A exposure in the mouse.

    DOI PubMed

  • Smooth muscle-associated protein 8: Distribution and biological activity in the rat brain

    G. Cristina Brailoiu, Siok L. Dun, Keisuke Mizuo, Eugen Brailoiu, Jun Yang, Jaw Kang Chang, Nae J. Dun

    JOURNAL OF NEUROSCIENCE RESEARCH ( WILEY-LISS )  85 ( 8 ) 1789 - 1796  2007.06  [Refereed]

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    With the use of an antiserum directed against the human smooth muscle-associated protein 8 (SMAP8) fragment SMAP898-138, Western blot and immunohistochemical studies revealed SMAP8 expression in the rat brain. A band with a molecular size of about 45 kDa was detected in tissues from the rat hypothalamus and a weaker band from the cortex. SMAP8 immunoreactivity (irSMAP8) was detected in neurons of the hypothalamic paraventricular, supraoptic, and supraoptic retrochiasmatic nuclei; a few irSMAP8 cells were scattered in the zona incerta as well as the cerebral cortex. Immunoreactive cell processes were detected mostly in the internal layer of the median eminence. Double labeling the hypothalamic sections with SMAP8 and vasopressin (VP) or oxytocin (OT) antiserum revealed that a population of VP- and OT-immunoreactive neurons expressed irSMAP8. The biological activity of SMAP8 in rat central neurons was assessed by the calcium microfluorimetric Fura-2 method. SMAP8 (100 nM) elevated cytosolic calcium concentrations [Ca2+](i) in a population of dissociated and cultured rat hypothalamic neurons; the response was eliminated in Ca2+-free saline. This is the first evidence of irSMAP8 in a population of MOT-containing hypothalamic neurons in the rat, and the peptide is biologically active in hypothalamic neurons, as evidenced by-mobilization of extracellular Ca2+. (c) 2007 Wiley-Liss, Inc.

    DOI PubMed

  • Distribution and characterization of estrogen receptor G protein-coupled receptor 30 in the rat central nervous system

    Eugen Brailoiu, Siok L. Dun, G. Cristina Brailoiu, Keisuke Mizuo, Larry A. Sklar, Tudor I. Oprea, Eric R. Prossnitz, Nae J. Dun

    JOURNAL OF ENDOCRINOLOGY ( SOC ENDOCRINOLOGY )  193 ( 2 ) 311 - 321  2007.05  [Refereed]

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    The G protein-coupled receptor 30 (GPR 30) has been identified as the non-genomic estrogen receptor, and G-1, the specific ligand for GPR30. With the use of a polyclonal antiserum directed against the human C-terminus of GPR30, immunohistochemical studies revealed GPR30-immuno-reactivity (irGPP30) in the brain of adult male and nonpregnant female rats. A high density of irGPR30 was noted in the Islands of Calleja and striaturn. In the hypothalamus, irGPR30 was detected in the paraventricular nucleus and supraoptic nucleus. The anterior and posterior pituitary contained numerous irGPR30 cells and terminal-like endings. Cells in the hippocampal formation as well as the substantia nigra were irGPR30. In the brainstem, irGPR30 cells were noted in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus of the vagus; a cluster of cells were prominently labeled in the nucleus ambiguus. Tissue sections processed with pre-immune serum showed no irGPR30, affirming the specificity of the antiserum. G-1 (100 nM) caused a large increase of intracellular calcium concentrations [Ca2+](i) in dissociated and cultured rat hypothalamic neurons, as assessed by microfluorometric Fura-2 imaging. The calcium response to a second application of G-1 showed a marked homologous desensitization. Our result shows a high expression of irGPR30 in the hypothalamic-pituitary axis, hippocampal formation, and brainstem autonomic nuclei; and the activation of GPR30 by G-1 is associated with a mobilization of calcium in dissociated and cultured rat hypothalamic neurons.

    DOI PubMed

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Misc 【 display / non-display 】

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Awards 【 display / non-display 】

  • 奨励賞

    2003   ニコチン・薬物依存研究フォーラム  

    Winner： 水尾圭祐

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Research Projects 【 display / non-display 】

  • Molecular mechanisms of ethanol dependence and relapse-role in the brain microRNA

    Grant-in-Aid for Young Scientists (B)

    Project Year :

    2009
    　
    　
     

    MIZUO Keisuke

    　View Summary

    Prolonged ethanol intake leads to the development of ethanol dependence. Although a lot of study suggested several candidates, certain mechanism of ethanol action is still unclear. Here we show that acute ethanol administration increased the expression of microRNA in mouse brain at 12 hours after administration. We observed that the acute ethanol administration significantly increased the levels of acetylated histone H3 in nucleus accumbens, ventral tegmental area and amygdala. The expression of miR-124 was significantly increased in limbic forebrain and lower midbrain following chronic treatment of ethanol. These findings suggest that chronic ethanol consumption increase the microRNA expression via histone acetylation, resulting in development of ethanol dependence.

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Presentations 【 display / non-display 】

  • Prenatal exposure to titanium dioxide nanoparticles alters brain monoamine concentration in mice

    Keisuke Mizuo, Yuta Takahashi, Ken Takeda

    Neuroscience 2009 

    Presentation date： 2009.10

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