Details of a Researcher - Okano, Hideyuki

Papers - Okano, Hideyuki

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Comparative study of different administrations of the neural stem cells for spinal cord injury in mice

Takahashi, Yuichiro, Nakamura, Masaya, Tuji, Osahiko, Kumagai, Gentarou, Hara, Chikako, Toyama, Yoshiaki, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S85 - S85 2008

Research paper (scientific journal), ISSN 0168-0102

In vitro and vivo characterization in human neural stem/progenitor cells expressing ABC transporter ABCB1

Kanemura, Yonehiro, Yamamoto, Atsuyo, Shofuda, Tomoko, Nakamura, Yasuhiro, Okano, Hideyuki, Yamasaki, Mami

NEUROSCIENCE RESEARCH 61 S86 - S86 2008

Research paper (scientific journal), ISSN 0168-0102

Functional analysis of Hu-associated RNA binding protein-network

Okano, Hirotaka J., Kakumoto, Kyoko, Igarashi, Maria, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S42 - S42 2008

Research paper (scientific journal), ISSN 0168-0102

The effect of anti-interleukin-6 receptor antibody in noise induced damaged cochlea

Wakabayashi, Kenichiro, Fujioka, Masato, Kanzaki, Sho, Yamashita, Daisuke, Masuda, Masatsugu, Okano, James Hirotaka, Okano, Hideyuki, Ogawa, Kaoru

NEUROSCIENCE RESEARCH 61 S102 - S102 2008

Research paper (scientific journal), ISSN 0168-0102

The functional analysis of RNA-binding protein Musashi2 in the cerebellum

Kuwako, Kenichiro, Shibata, Shinsuke, Okano, Hirotaka J., Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S89 - S89 2008

Research paper (scientific journal), ISSN 0168-0102

Investigation of neural crest stem cell therapy for Hirschsprung's disease

Shimojima, Naoki, Morikawa, Yasuhide, Hotta, Ryo, Nagoshi, Narihito, Shibata, Shinsuke, Okano, James Hirotaka, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S36 - S36 2008

Research paper (scientific journal), ISSN 0168-0102

SOCS3 is required to protect photoreceptor cell function during retinal inflammation

Ozawa, Yoko, Nakao, Keiko, Kurihara, Trishilhide, Shimazaki, Takuya, Shimmura, Shigeto, Ishida, Susumu, Yoshimura, Akihiko, Tsubota, Kazuo, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S269 - S269 2008

Research paper (scientific journal), ISSN 0168-0102

Neural RNA-binding protein Musashi1 inhibits translation initiation by competing with eIF4G for PABP

Kawahara, Hironori, Imai, Takao, Imataka, Hiroaki, Tujimoto, Masafumi, Matsumoto, Ken, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S153 - S153 2008

Research paper (scientific journal), ISSN 0168-0102

Anti IL-6 antibody treatment reduces the infiltration of hematogenous macrophages into the injured spinal cord

Mukaino, Masahiko, Nakamura, Masaya, Yamada, Osama, Okada, Seiji, Morikawa, Satoru, Osugi, Yoshiyuki, Matsuzaki, Yumi, Toyama, Yoshiaki, Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S275 - S275 2008

Research paper (scientific journal), ISSN 0168-0102

A role of neuronal RNA-binding protein Hu and NF45/90 in the nervous system

Igarashi, Mania, Yano, Masato, Okano, Hirotaka J., Okano, Hideyuki

NEUROSCIENCE RESEARCH 61 S153 - S153 2008

Research paper (scientific journal), ISSN 0168-0102

Expression of free fatty acid receptor GPR40 in the neurogenic niche of adult monkey hippocampus

Ma, Dexuan, Lu, Li, Boneva, Nadezhda B., Warashina, Shogo, Kaplamadzhiev, Desislav B., Mori, Yoshimi, Nakaya, Masa-aki, Kikuchi, Mitsuru, Tonchev, Anton B., Okano, Hideyuki, Yamashima, Tetsurnori

HIPPOCAMPUS 18 ( 3 ) 326 - 333 2008

Research paper (scientific journal), ISSN 1050-9631

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Mature Adipocyte-Derived Cells, Dedifferentiated Fat Cells (DFAT), Promoted Functional Recovery From Spinal Cord Injury-Induced Motor Dysfunction in Rats

Ohta, Yuki, Takenaga, Mitsuko, Tokura, Yukie, Hamaguchi, Akemi, Matsumoto, Taro, Kano, Koichiro, Mugishima, Hideo, Okano, Hideyuki, Igarashi, Rie

CELL TRANSPLANTATION 17 ( 8 ) 877 - 886 2008

Research paper (scientific journal), ISSN 0963-6897

In vivo imaging in humanized mice

Masuda H., Okano H. J., Maruyama T., Yoshimura Y., Okano H., Matsuzaki Y.

Current topics in microbiology and immunology 324 179 - 196 2008

ISSN 0070-217X

The radiological modalities that are currently utilized as critical components in clinical medicine have also been adapted to small-animal imaging, among which are ultrasound imaging, X-ray computerized tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), and singlephoton emission computed tomography (SPECT). Optical imaging techniques such as bioluminescence imaging (BLI) and fluorescence imaging (FLI) are approaches that are commonly used in small animals. Longitudinal surveys of living (i.e., nonsacrificed) animal models with these modalities provide some clues for the development of clinical applications. The techniques are absolutely essential for translational research. However, there are currently few tools available with sufficient spatial or temporal resolution ideal for all experimental studies. In this chapter, we provide a rationale and techniques for visualizing target cells in living small animals and an overview of the advantages and limitations of current imaging technology. Finally, we introduce a humanized mouse and a novel in vivo imaging system that we have developed. We also discuss real-time observations of reconstructs and clinical manifestations. © 2008 Springer-Verlag.

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Structural analysis of Musashi-RNA complex on the basis of long-range structural information.

Ohyama Takako, Furukawa Ayako, Mashima Tsukasa, Sugiyama Takashi, Ohgara Shouta, Yamazaki Toshio, Imai Takao, Okano Hideyuki, Nagata Takashi, Katahira Masato

Nucleic acids symposium series (2004) ( 52 ) 193 - 194 2008

Musashi protein is supposed to be involved in the regulation of differentiation of neural stem cells. Musashi binds to 3' untranslated region of target mRNA and represses the translation of mRNA. Musashi has two tandem RNA-binding domains (RBDs), RBD1 and RBD2. Both RBDs cooperatively bind to the target mRNA. Here, we determined the structure of RBD1-RBD2 in complex with target RNA. First, the structures of two RBDs in the complex were determined on the basis of short-range distance restrains derived from NOEs. However, the relative position of two RBDs was not determined due to the lack of long-range distance restraints across two RBDs. In order to overcome the situation, we introduced the paramagnetic center into Musashi by attaching MTSL carrying the NO radical. The long-range distance restraints (ca. 20-40 A) between two RBDs were derived from paramagnetic relaxation enhancement (PRE) caused by the paramagnetic center. The relative position of two RBDs was successfully determined on the basis of these long-range distance restraints. The change in the relative position of two RBDs on binding to the target RNA was also detected by PRE. The determined structure of RBD1-RBD2 in the complex has suggested how Musashi recognizes its target mRNA.

Mature adipocyte-derived cells, dedifferentiated fat cells (DFAT), promoted functional recovery from spinal cord injury-induced motor dysfunction in rats

Ohta Yuki, Takenaga Mitsuko, Tokura Yukie, Hamaguchi Akemi, Matsuraoto Taro, Kano Koichiro, Mugishima Hideo, Okano Hideyuki, Igarashi Rie

Cell Transplantation 17 ( 8 ) 877 - 886 2008

ISSN 0963-6897

Transplantation of mature adipocyte-derived cells (dedifferentiated fat cells) led to marked functional recovery from spinal cord injury (SCI)-induced motor dysfunction in rats. When mature adipocytes were isolated from rat adipose tissue and grown in ceiling culture, transformation into fibroblast-like cells without lipid droplets occurred. These fibroblast-like cells, termed dedifferentiated fat cells (DFAT), could proliferate and could also differentiate back into adipocytes. DFAT expressed neural markers such as nestin, βIII tubulin, and GFAP. Allografting of DFAT into SCI-induced rats led to significant recovery from hindlimb dysfunction. Grafted cells were detected at the injection site, and some of these cells expressed βIII tubulin. DFAT expressed neurotrophic factors such as BDNF and GDNF prior to transplantation, and grafted cells were also positive for these factors. Therefore, these neurotrophic factors derived from grafted DFAT might have contributed to the promotion of functional recovery. These findings also suggest that mature adipocytes could become a new source for cell replacement therapy to treat central nervous system disorders. Copyright © 2008 Cognizant Comm. Corp.

Notch-Hes1 Pathway Contributes to the Cochlear Prosensory Formation Potentially Through the Transcriptional Down-Regulation of p27(Kip1)

Murata, Junko, Ohtsuka, Toshiyuki, Tokunaga, Akinori, Nishiike, Suetaka, Inohara, Hidenori, Okano, Hideyuki, Kageyama, Ryoichiro

JOURNAL OF NEUROSCIENCE RESEARCH 87 ( 16 ) 3521 - 3534 2009.12

Research paper (scientific journal), ISSN 0360-4012

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Preimplantation Development of Somatic Cell Cloned Embryos in the Common Marmoset (Callithrix jacchus)

Sotomaru, Yusuke, Hirakawa, Reiko, Shimada, Akiko, Shiozawa, Seiji, Sugawara, Ayako, Oiwa, Ryo, Nobukiyo, Asako, Okano, Hideyuki, Tamaoki, Norikazu, Nomura, Tatsuji, Hiyama, Eiso, Sasaki, Erika

CLONING AND STEM CELLS 11 ( 4 ) 575 - 583 2009.12

Research paper (scientific journal), ISSN 1536-2302

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Transplantation of dendritic cells promotes functional recovery from spinal cord injury in common marmoset

Yaguchi, Masae, Tabuse, Masanao, Ohta, Shigeki, Ohkusu-Tsukada, Kozo, Takeuchi, Tamaki, Yamane, Junichi, Katoh, Hiroyuki, Nakamura, Masaya, Matsuzaki, Yumi, Yamada, Masayuki, Itoh, Toshio, Nomura, Tatsuji, Toyama, Yoshiaki, Okano, Hideyuki, Toda, Masahiro

NEUROSCIENCE RESEARCH 65 ( 4 ) 384 - 392 2009.12

Research paper (scientific journal), ISSN 0168-0102

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Neuronal re-juvenilization in the nucleus ambiguus after vagal nerve injury

Takaoka, Takuji, Shiotani, Akihiro, Saito, Koichiro, Tomifuji, Masayuki, Mori, Yuko, Fujimine, Takekatsu, Okano, Hideyuki, Ogawa, Kaoru

NEUROSCIENCE RESEARCH 65 ( 4 ) 353 - 359 2009.12

Research paper (scientific journal), ISSN 0168-0102

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Reconsideration of Insulin Signals Induced by Improved Laboratory Animal Diets, Japanese and American Diets, in IRS-2 Deficient Mice

Hashimoto H., Arai T., Mori A., Kawai K., Hikishima K., Ohnishi Y., Eto T., Ito M., Hioki K., Suzuki R., Ohsugi M., Saito M., Ueyama Y., Okano H., Yamauchi T., Kubota N., Ueki K., Tobe K., Tamaoki N., Kadowaki T., Kosaka K.

Experimental and Clinical Endocrinology and Diabetes 117 ( 10 ) 577 - 586 2009.11

ISSN 0947-7349

Current Japanese and American diets and Japanese diet immediately after the War were converted to laboratory animal diets. As a result, current laboratory animal diet (CA-I, CLEA) unexpectedly resembled the diet of Japanese after the War. This is considered to result in an under-evaluation of diabetes research using laboratory animals at present. Therefore, changes in insulin signals caused by current Japanese and American diets were examined using IRS-2 deficient mice (Irs2 ^-/- mice) and mechanisms of aggravation of type 2 diabetes due to modern diets were examined. Irs2 ^-/- mice at 6 weeks of age were divided into three groups: Japanese diet (Jd) group, American diet (Ad) group and CA-I diet [regular diet (Rd)] group. Each diet was given to the dams from 7 days before delivery. When the Irs2 ^-/- mice reached 6 weeks of age, the glucose tolerance test (GTT), insulin tolerance test (ITT) and organ sampling were performed. The sampled organs and white adipose tissue were used for analysis of RNA, enzyme activity and tissues. In GTT and ITT, the Ad group showed worse glucose tolerance and insulin resistance than the Rd group. Impaired glucose tolerance of the Jd group was the same as that of the Rd group, but insulin resistance was worse than in the Rd group. These results were caused an increase in fat accumulation and adipocytes in the peritoneal cavity by lipogenic enzyme activity in the liver and muscle, and the increase in TNFa of hypertrophic adipocyte origin further aggravated insulin resistance and the increase in resistin also aggravated the impaired glucose tolerance, leading to aggravation of type 2 diabetes. The Japanese and American diets given to the Irs2 ^-/- mice, which we developed, showed abnormal findings in some Irs2 ^-/- mice but inhibited excessive reactions of insulin signals as diets used in ordinary nutritional management.

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