Updated on 2022/07/26

写真a

 
KAMIYA Atsunori
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Professor
Position
Professor
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Degree

  • 博士(医学) ( 2000.1   名古屋大学 )

  • PhD, MD ( 2000.1   Nagoya University )

Research Areas

  • Life Science / Physiology

  • Life Science / Biomedical engineering

  • Life Science / Neuroscience-general

Committee Memberships

  • 日本学術振興会   特別研究員等審査会専門委員  

    2017 - 2018   

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    Committee type:Government

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  • 新エネルギー産業技術総合開発機構   テーマ公募型事業事前評価委員  

    2005   

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    Committee type:Government

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Papers

  • Upregulation of Mir342 in Diet-Induced Obesity Mouse and the Hypothalamic Appetite Control

    Dongxiao Zhang, Satoshi Yamaguchi, Xinhao Zhang, Boxuan Yang, Naoko Kurooka, Ryosuke Sugawara, Haya Hamed H. Albuayjan, Atsuko Nakatsuka, Jun Eguchi, Takeshi Y. Hiyama, Atsunori Kamiya, Jun Wada

    Frontiers in Endocrinology   12   2021.8

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    Publishing type:Research paper (scientific journal)  

    In obesity and type 2 diabetes, numerous genes are differentially expressed, and microRNAs are involved in transcriptional regulation of target mRNAs, but miRNAs critically involved in the appetite control are not known. Here, we identified upregulation of miR-342-3p and its host gene Evl in brain and adipose tissues in C57BL/6 mice fed with high fat-high sucrose (HFHS) chow by RNA sequencing. Mir342 (-/-) mice fed with HFHS chow were protected from obesity and diabetes. The hypothalamic arcuate nucleus neurons co-express Mir342 and EVL. The percentage of activated NPY+pSTAT3+ neurons were reduced, while POMC+pSTAT3+ neurons increased in Mir342 (-/-) mice, and they demonstrated the reduction of food intake and amelioration of metabolic phenotypes. Snap25 was identified as a major target gene of miR-342-3p and the reduced expression of Snap25 may link to functional impairment hypothalamic neurons and excess of food intake. The inhibition of miR-342-3p may be a potential candidate for miRNA-based therapy.

    DOI: 10.3389/fendo.2021.727915

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  • Adrenergic signaling promotes the expansion of cancer stem-like cells of malignant peripheral nerve sheath tumors

    Rongsheng Huang, Atsushi Fujimura, Eiji Nakata, Shota Takihira, Hirofumi Inoue, Soichiro Yoshikawa, Takeshi Hiyama, Toshifumi Ozaki, Atsunori Kamiya

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   557   199 - 205   2021.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Malignant peripheral nerve sheath tumor (MPNST), a highly malignant tumor that arises in peripheral nerve tissues, is known to be highly resistant to radiation and chemotherapy. Although there are several reports on genetic mutations and epigenetic changes that define the pathogenesis of MPNST, there is insufficient information regarding the microenvironment that contributes to the malignancy of MPNST. In the present study, we demonstrate that adrenaline increases the cancer stem cell population in MPNST. This effect is mediated by adrenaline stimulation of beta-2 adrenergic receptor (ADRB2), which activates the Hippo transducer, YAP/TAZ. Inhibition and RNAi experiments revealed that inhibition of ADRB2 attenuated the adrenaline-triggered activity of YAP/TAZ and subsequently attenuated MPNST cells stemness. Furthermore, ADRB2-YAP/TAZ axis was confirmed in the MPNST patients' specimens. The prognosis of patients with high levels of ADRB2 was found to be significantly worse. These data show that adrenaline exacerbates MPNST prognosis and may aid the development of new treatment strategies for MPNST.(c) 2021 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

    DOI: 10.1016/j.bbrc.2021.03.172

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  • The role of basophils in acquired protective immunity to tick infestation

    Soichiro Yoshikawa, Kensuke Miyake, Atsunori Kamiya, Hajime Karasuyama

    PARASITE IMMUNOLOGY   43 ( 5 )   2021.5

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    Language:English   Publisher:WILEY  

    Ticks are blood-feeding ectoparasites that transmit a variety of pathogens to host animals and humans, causing severe infectious diseases such as Lyme disease. In a certain combination of animal and tick species, tick infestation elicits acquired immunity against ticks in the host, which can reduce the ability of ticks to feed on blood and to transmit pathogens in the following tick infestations. Therefore, our understanding of the cellular and molecular mechanisms of acquired tick resistance (ATR) can advance the development of anti-tick vaccines to prevent tick infestation and tick-borne diseases. Basophils are a minor population of white blood cells circulating in the bloodstream and are rarely observed in peripheral tissues under steady-state conditions. Basophils have been reported to accumulate at tick-feeding sites during re-infestation in cattle, rabbits, guinea pigs and mice. Selective ablation of basophils resulted in a loss of ATR in guinea pigs and mice, illuminating the essential role of basophils in the manifestation of ATR. In this review, we discuss the recent advance in the elucidation of the cellular and molecular mechanisms underlying basophil recruitment to the tick-feeding site and basophil-mediated ATR.

    DOI: 10.1111/pim.12804

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  • Differentiated glioblastoma cells accelerate tumor progression by shaping the tumor microenvironment via CCN1-mediated macrophage infiltration

    Atsuhito Uneda, Kazuhiko Kurozumi, Atsushi Fujimura, Kentaro Fujii, Joji Ishida, Yosuke Shimazu, Yoshihiro Otani, Yusuke Tomita, Yasuhiko Hattori, Yuji Matsumoto, Nobushige Tsuboi, Keigo Makino, Shuichiro Hirano, Atsunori Kamiya, Isao Date

    ACTA NEUROPATHOLOGICA COMMUNICATIONS   9 ( 1 )   2021.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:BMC  

    Glioblastoma (GBM) is the most lethal primary brain tumor characterized by significant cellular heterogeneity, namely tumor cells, including GBM stem-like cells (GSCs) and differentiated GBM cells (DGCs), and non-tumor cells such as endothelial cells, vascular pericytes, macrophages, and other types of immune cells. GSCs are essential to drive tumor progression, whereas the biological roles of DGCs are largely unknown. In this study, we focused on the roles of DGCs in the tumor microenvironment. To this end, we extracted DGC-specific signature genes from transcriptomic profiles of matched pairs of in vitro GSC and DGC models. By evaluating the DGC signature using single cell data, we confirmed the presence of cell subpopulations emulated by in vitro culture models within a primary tumor. The DGC signature was correlated with the mesenchymal subtype and a poor prognosis in large GBM cohorts such as The Cancer Genome Atlas and Ivy Glioblastoma Atlas Project. In silico signaling pathway analysis suggested a role of DGCs in macrophage infiltration. Consistent with in silico findings, in vitro DGC models promoted macrophage migration. In vivo, coimplantation of DGCs and GSCs reduced the survival of tumor xenograft-bearing mice and increased macrophage infiltration into tumor tissue compared with transplantation of GSCs alone. DGCs exhibited a significant increase in YAP/TAZ/TEAD activity compared with GSCs. CCN1, a transcriptional target of YAP/TAZ, was selected from the DGC signature as a candidate secreted protein involved in macrophage recruitment. In fact, CCN1 was secreted abundantly from DGCs, but not GSCs. DGCs promoted macrophage migration in vitro and macrophage infiltration into tumor tissue in vivo through secretion of CCN1. Collectively, these results demonstrate that DGCs contribute to GSC-dependent tumor progression by shaping a mesenchymal microenvironment via CCN1-mediated macrophage infiltration. This study provides new insight into the complex GBM microenvironment consisting of heterogeneous cells.

    DOI: 10.1186/s40478-021-01124-7

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  • In Vitro Studies to Define the Cell-Surface and Intracellular Targets of Polyarginine-Conjugated Sodium Borocaptate as a Potential Delivery Agent for Boron Neutron Capture Therapy

    Atsushi Fujimura, Seiji Yasui, Kazuyo Igawa, Ai Ueda, Kaori Watanabe, Tadashi Hanafusa, Yasuaki Ichikawa, Sachiko Yoshihashi, Kazuki Tsuchida, Atsunori Kamiya, Shuichi Furuya

    CELLS   9 ( 10 )   2020.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:MDPI  

    Boron neutron capture therapy (BNCT) requires pharmaceutical innovations and molecular-based evidence of effectiveness to become a standard cancer therapeutic in the future. Recently, in Japan, 4-borono-L-phenylalanine (BPA) was approved as a boron agent for BNCT against head and neck (H&N) cancers. H&N cancer appears to be a suitable target for BPA-BNCT, because the expression levels of L-type amino acid transporter 1 (LAT1), one of the amino acid transporters responsible for BPA uptake, are elevated in most cases of H&N cancer. However, in other types of cancer including malignant brain tumors, LAT1 is not always highly expressed. To expand the possibility of BNCT for these cases, we previously developed poly-arginine peptide (polyR)-conjugated mercaptoundecahydrododecaborate (BSH). PolyR confers the cell membrane permeability and tumor selectivity of BSH. However, the molecular determinants for the properties are not fully understood. In this present study, we have identified the cluster of differentiation 44 (CD44) protein and translational machinery proteins as a major cell surface target and intracellular targets of BSH-polyR, respectively. CD44, also known as a stem cell-associated maker in various types of cancer, is required for the cellular uptake of polyR-conjugated molecules. We showed that BSH-polyR was predominantly delivered to a CD44(High) cell population of cancer cells. Once delivered, BSH-polyR interacted with the translational machinery components, including the initiation factors, termination factors, and poly(A)-biding protein (PABP). As a proof of principle, we performed BSH-polyR-based BNCT against glioma stem-like cells and revealed that BSH-polyR successfully induced BNCT-dependent cell death specifically in CD44(High) cells. Bioinformatics analysis indicated that BSH-polyR would be suitable for certain types of malignant tumors. Our results shed light on the biochemical properties of BSH-polyR, which may further contribute to the therapeutic optimization of BSH-BNCT in the future.

    DOI: 10.3390/cells9102149

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Books

  • 細胞はどのように力を感知して利用するのか?I.感覚系のメカノセンシング 3.神経系による血圧調節

    神谷厚範

    実験医学 38(7)  2020 

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MISC

 

Class subject in charge

  • Human Physiology (2021academic year) Concentration  - その他

  • Medical Tutorial (2021academic year) 1st semester  - 火2~3

  • Medical Tutorial (2021academic year) 1st semester  - 火2~3

  • Physiology (1) (2021academic year) special  - その他

  • Practice in Physiology (1) (2021academic year) special  - その他

  • Research Projects and Practicals: Cellular Physiology I (2021academic year) special  - その他

  • Lecture and Research Projects: Cellular Physiology I (2021academic year) special  - その他

  • Research Projects and Practicals: Cellular Physiology II (2021academic year) special  - その他

  • Lecture and Research Projects: Cellular Physiology II (2021academic year) special  - その他

  • Research Presentation in Cell and Tissue Engineering (2021academic year) special  - その他

  • Practice in Physiology (1) (2020academic year) special  - その他

  • Physiology (1) (2020academic year) special  - その他

  • Research Projects and Practicals: Cellular Physiology I (2020academic year) special  - その他

  • Lecture and Research Projects: Cellular Physiology I (2020academic year) special  - その他

  • Research Projects and Practicals: Cellular Physiology II (2020academic year) special  - その他

  • Lecture and Research Projects: Cellular Physiology II (2020academic year) special  - その他

  • Research Presentation in Cell and Tissue Engineering (2020academic year) Year-round  - その他

  • Cell and Tissue Engineering (2020academic year) Year-round  - その他

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