Okano, Hideyuki

写真a

Affiliation

University (Mita)

Position

Professor (Non-tenured)

Related Websites

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Research Areas 【 Display / hide 】

  • Life Science / Molecular biology (Molecular Biology)

  • Life Science / Developmental biology (Developmental Biology)

  • Life Science / Neuroscience-general (General Neuroscience)

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Research Themes 【 Display / hide 】

  • Development and regeneration of central nervous system, 

    1983
    -
    Present

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Books 【 Display / hide 】

  • 新世紀の精神科治療・第6巻

    '多田敬典,　岡野栄之', 2003.05

    Scope: 219-229

  • 脳神経科学

    '徳永暁憲,　岡野栄之', 2003.05

    Scope: 167-176

  • Chapter 18. Neuron Regeneration Using iPS Cells.

    OKANO HIDEYUKI, Science Publishers, CRC Press, Boca Raton, FL,, 2013

    Scope: 315-332

  • Transplantation of neural stem cells for spinal cord regeneration.

    OKANO HIDEYUKI, Springer-Verlag (Heidelberg, Germany), 2008

  • Functions of neural RNA-binding proteins Musashi and Hu in stem cells and neuronal differentiation.

    OKANO HIDEYUKI, Research Signpost, Kerala, India,, 2008

    Scope: 107-121

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Papers 【 Display / hide 】

  • Disorders in myelination in the twitcher mutant

    Mikoshiba Katsuhiko, Fujishiro Masatoshi, Kohsaka Shinichi, Okano Hideyuki, Takamatsu Ken, Tsukada Yasuzo

    Neurochemical Research 10 ( 8 ) 1129 - 1141 1985.08

    ISSN  0364-3190

    　View Summary

    <p>The twitcher is an autosomal recessive mutant mouse characterized by absence of galactosylceramidase. The twitcher shows clinical and histological features similar to those of human Krabbe-type leukodystrophy. We here present the results of a neurochemical and immunohistochemical analysis of the twitcher. Electrophoretic analysis revealed that in the particulate fraction of the spinal cord, myelin basic proteins (MBP) and proteolipid protein were decreased, and in the sciatic nerve fibers, PO protein, X, Y and MBP were clearly decreased. 2′,3′-Cyclic nucleotide 3′-phosphodiesterase (CNPase) activities of the pallium cerebri, brain stem and spinal cord of the twitcher were about 20% less than those of the control. However, in the sciatic nerve, the activity was half that of the control. Immunohistochemical studies were carried out by means of antisera against MBP and CNPase. There were clear patches indicating both MBP- and CNPase-negative reactions in the white matter of the central nervous system from the twitcher. The reaction on the section of sciatic nerve fibers from the twitcher showed a positive reaction only in a very limited number of fibers with both MBP and CNPase antisera. A clear astrocytic hypertrophy was detected by the antiserum against glial fibrillary acidic protein (GFAP). Even in the grey matter of the cerebral cortex, strong GFAP-positive astrocytes were clearly observed. © 1985 Plenum Publishing Corporation.</p>

  • Molecular genetic analysis of myelin-deficient mice: shiverer mutant mice show deletion in gene(s) coding for myelin basic protein.

    1) Kimura M, Inoko H, Katsuki M, Ando, A, Sato T, Hirose T, Takashima H, Inayama S, Okano H, Takamatsu K, Mikoshiba K, Tsukada Y, Watanabe I.

    Journal of Neurochemistry 44   692 - 696 1985

    Research paper (scientific journal), Joint Work, Accepted

    　View Summary

    The gene expression of myelin basic proteins (MBPs) in shiverer mutant mice was investigated by the Northern and Southern hybridization techniques. In the control mice RNA molecules from the brains which were about 2,300 nucleotides in length were hybridized to cDNA of 1.8 kb encoding for a mouse MBP, but RNA from the brains of 3-week-old shiverer mutant mice contained no detectable amount of MBP transcripts hybridizing to this probe. Moreover the shiverer mutant mice lost several restriction fragments that hybridized to the same probe in the control mice when each of the five restriction enzymes, i.e., HindIII, PstI, PvuII, AccI, and StuI, was used. These data suggest that the shiverer mutation may correspond to the deletion of a large portion of MBP exon(s) in the gene, and this deletion causes inefficient transcription leading to the depletion of MBPs in the myelin and the dysmyelination observed in these mice.

  • P400 protein characteristic to Purkinje cells and related proteins in cerebella from neuropathological mutant mice

    Mikoshiba K., Okano H., Tsukada Y.

    Developmental Neuroscience 7 ( 3 ) 179 - 187 1985

    ISSN  0378-5866

    　View Summary

    <p>P400 protein has been found in the cerebellum and localizes to Purkinje cells. It is a glycoprotein and reacts with plant lectins. Autoradiographic patterns of the protein profiles of mutant mice cerebella after intracranial injections of 14C-leucine were analyzed. P400 protein was one of the dominant proteins labeled in the control cerebellum. No incorporation of 14C-leucine to the position of P400 protein was found in the nervous and pcd mutant mice where no Purkinje cells and no P400 protein are present. P400 protein in weaver cerebellum was labelled more intensely than that in the control. In the staggerer mice, where dendritic arborization of Purkinje cell is poor and no spines are formed on the dendrites, no P400 protein was found and no 14C-leucine incorporation was observed to the position of P400 protein, suggesting that staggerer is a mutation where no P400 protein accumulated in the fractions being studied. P400 protein was phosphorylated independently of the presence of Ca2+. Among the proteins of the isolated Purkinje cells, P400 protein was one of the major proteins phosphorylated.</p>

  • Immunohistochemical, biochemical and electron microscopic analysis of myelin formation in the central nervous system of myelin deficient (mld) mutant mice.

    Mikoshiba K., Okano H., Inoue Y., Fujishiro M., Takamatsu K., Lachapelle F., Baumann N., Tsukada Y.

    Brain Research 432 ( 1 ) 111 - 121 1987.09

    ISSN  0006-8993

    　View Summary

    <p>Myelin deficiency (mld) is an autosomal recessive mutation in mice and is considered to be allelic to the shiverer (shi) mutation. Mld mice are characterized by hypomyelination of the central nervous system (CNS). They show typical symptoms such as tremor, tonic convulsion and ataxic movement. Subcellular fractionation of the CNS revealed that the MBP bands were greatly decreased in the P2A (myelin) fraction and the total content of myelin basic protein (MBP) was much lower than that in the control in all parts of the CNS. Sections from mld mice were examined by immunohistochemical tests with MBP antiserum, and a mosaic expression of MBP was found in the myelin of the mld mice. Since the major dense line is considered to be composed mainly of MBP, we investigated the myelin of mld mice by electron microscopy and found that there were 3 types of myelin: (1) a normal type compact myelin with a major dense line, (2) a shiverer-type myelin with no major dense line, and (3) a mixed-type myelin, in which within a myelin lamella the major dense line abruptly changes to cytoplasm of oligodendrocytes.</p>

  • Inefficient transcription of the myelin basic protein gene possibly causes hypomyelination in myelin-deficient mutant mice

    Okano H., Miura M., Moriguchi A., Ikenaka K., Tsukada Y., Mikoshiba K.

    Journal of Neurochemistry 48 ( 2 ) 470 - 476 1987

    ISSN  0022-3042

    　View Summary

    <p>A hereditary dysmyelination mutation, named myelin deficient (mld), is considered to be allelic to shiverer, a deletion mutation of the myelin basic protein (MBP) gene. The present study showed that MBP expression is greatly reduced in mld, but that it is still detectable. Northern blot analysis revealed that the pronounced decrease in the MBP level in mld resulted from a reduced mRNA level and was not caused by deletion of a large portion of the MBP gene as in shiverer. Southern blod studies with BamHI-digested chromosomal DNA suggested some part of the MBP gene, at least the 5'-portion, was duplicated in mld. These results indicated that the mld and shiverer mutations were different from each other, even though genetic allelism between the two was reconfirmed. We also examined the developmental pattern of the gene expression of MBP and that of another protein, myelin proteolipid protein (PLP), specifically expressed in the oligodendrocyte, in mld by RNA dot blot study. The mRNA level of MBP in mld was greatly reduced during the active myelination stages, gradually increasing and remaining constant in the later stages. The PLP-mRNA content in mld was almost normal (60-80% that of control) at any stage of development. All these findings imply that the primary defect in mld is due to reduced transcriptional activity of the MBP gene.</p>

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Papers, etc., Registered in KOARA 【 Display / hide 】

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Reviews, Commentaries, etc. 【 Display / hide 】

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Presentations 【 Display / hide 】

  • Self-renewal of neural stem cells and CNS repair

    Okano Hideyuki

    'Pre-Meeting Workshop:Neural Stem Cell Biology and Potential Therapeutic Applicaiton ''American Society for Neurochemictry''' ('California, USA') , 

    2003.05
    , 

    Oral presentation (invited, special)

  • Attempts toward the stem cell therapy for spinal cord injuries

    Okano Hideyuki

    IBRO World Congress of Neuroscience (Prague.Czech Republic) , 

    2003.07
    , 

    Oral presentation (invited, special)

  • Stem cells for neurodegenerative diseases

    Okano Hideyuki

    <Stem cells:From Genetics to Cell Therapy> An International Symposium sponsored by the Tore Nilsson and Marcus Wallenberg foundation ('Lund, Sweden') , 

    2003.09
    , 

    Oral presentation (invited, special)

  • Regulation of NOTCH signaling during proliferation and differentiation of postembryonic neuroblasts

    'Toriya Masako, Nakao Keiko, Okano Hideyuki'

    2003 Cold Spring Harbor Meeting on Neurology of Drosophila ('New York, USA') , 

    2003.10
    , 

    Poster presentation

  • tincar encodes a Drosophila novel transmembrane protein required for the morphogenesis of eye and the function of dorsal vessel

    'Hirota Yuki, Sawamoto Kazunobu, Ueda Ryu, Okano Hideyuki'

    New Horizons in Molecular Sciences and Systems: An Integrated Approach ('Nago, Japan') , 

    2003.10
    , 

    Poster presentation

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

  • Molecular mechanisms to avert motor neurons vu&#768;lnerabi&#769;lity in ALS

    2020.04
    -
    2024.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (A) , Principal investigator

  • ヒトiPS細胞と霊長類モデルを用いた治療開発の基盤整備

    2014.07
    -
    2019.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research on Innovative Areas, Principal investigator

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Works 【 Display / hide 】

  • 医学部国際交流委員会委員

    2003.10
    -
    2005.09
    , 

    Other

  • 国際交流委員会委員

    2001.10
    -
    2003.09
    , 

    Other

  • 学務委員会委員

    2001.10
    -
    2003.09
    , 

    Other

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Awards 【 Display / hide 】

  • Faculty Award for Internalization 2016 (Impact factor Most Outstanding Award)

    2016, 慶應義塾大学

  • Molecular Brain Award

    2016, The Association for the Study of Neurons and Diseases (A.N.D.)

  • 第51回ベルツ賞(1等賞)

    2014, 日本ベーリンガーインゲルハイム, 幹細胞を用いた脊髄損傷の再生医療

  • Stem Cell Innovator Award

    2013, GeneExpression Systems & Apasani Research Conference USA

  • The Johnson & Johnson Innovation Award

    2011, 日本再生医療学会

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Courses Taught 【 Display / hide 】

  • PHYSIOLOGY 2

    2024

  • MOLECULAR BIOLOGY 2

    2024

  • MEDICAL PROFESSIONALISM 3

    2024

  • MCB(MOLECULAR CELL BIOLOGY)

    2024

  • PHYSIOLOGY 2

    2023

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Courses Previously Taught 【 Display / hide 】

  • MEP3

    Keio University

    2017.04
    -
    2018.03
    , 

    Spring Semester, Lecture

  • 症例検討(幹細胞医学）

    Keio University

    2017.04
    -
    2018.03
    , 

    Lecture

  • 生理学実習

    Keio University

    2017.04
    -
    2018.03
    , 

    Full academic year, Laboratory work/practical work/exercise

  • 幹細胞医学

    Keio University

    2017.04
    -
    2018.03
    , 

    Full academic year, Lecture

  • 生理学Ⅱ

    Keio University

    2017.04
    -
    2018.03
    , 

    Full academic year, Lecture, 115people

    生理学概論　内分泌　

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