Updated on 2026/03/10

写真a

 
Hikita Takao
 
Organization
Scheduled update Special-Appointment Associate Professor
Position
Special-Appointment Associate Professor
Profile

[研究コンセプト]

臓器を形成する細胞は様々な手段でコミュニケーションを取り全身の恒常性を維持しています。一方、何らかの原因によってコミュニケーションに齟齬が生じると疾患の原因になりえます。私は臓器間コミュニケーションに関わる分子基盤を代謝性疾患の観点より明らかにする事で、新しい創薬標的の発見を目指しています。また、新規知見に基づき薬剤を開発し、収益化可能な知財を整備することにより、持続的な研究環境の構築を進めます。

 

[自己紹介]

大阪生まれの三重育ち。

 

[座右の銘]

Let's enjoy science

External link

Degree

  • PhD ( Nagoya University )

Research Interests

  • 再生医療

  • 細胞移動

  • 生化学

  • 遺伝学

  • 包括脳ネットワーク

  • プロテオーム

  • 低分子量GTPase

  • Proteomic analysis

  • Pharmacology

  • Cell polarity

Research Areas

  • Life Science / Genetics  / C. elegansを用いた低分子量Gタンパク質の機能解析

  • Life Science / Medical biochemistry  / 血管内皮細胞の極性と炎症

  • Life Science / Pharmacology  / 血管内皮細胞障害と糖尿病合併症

  • Life Science / Neuroscience-general  / 神経細胞移動・再生医療・精神疾患原因遺伝子

Education

  • 名古屋大学大学院   医学系研究科   博士課程

    2002.4 - 2006.3

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  • Nara Institute of Science and Technology   バイオサイエンス研究科   博士課程前期

    2000.4 - 2002.3

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  • Kagawa University   農学部   生物資源学科

    1996.4 - 2000.3

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Research History

  • Max Planck Institute for Heart and Lung Research   Guest scientist

    2022.12 - 2024.12

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  • Okayama University   Organization for Research Promotion & Collaboration

    2021.10

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  • マックスプランク心肺研究所   ポストドクトラルフェロー

    2014.4 - 2022.1

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  • Nagoya City University   Graduate School of Medical Sciences, Department of Developmental and Regenerative Biology   Assistant Professor

    2010.4 - 2013.3

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  • Nagoya City University   Graduate School of Medical Sciences, Department of Developmental and Regenerative Biology

    2009.4 - 2010.3

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  • 名古屋大学医学部 神経情報薬理学講座   ポストドクトラルフェロー

    2006.4 - 2009.3

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Professional Memberships

Committee Memberships

  • 日本血管生物医学会   評議員  

    2022.12   

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    Committee type：Academic society

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Papers

  • Complex relationship among vessel diameter, shear stress and blood pressure controlling vessel pruning during angiogenesis. Reviewed International journal

    Vivek Kumar, Yosuke Hasegawa, Prashant Kumar, Takao Hikita, Mingqian Ding, Yukinori Kametani, Masanori Nakayama

    PLoS computational biology   22 ( 1 )   e1013565   2026.1

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    Blood vessel pruning during angiogenesis is the optimization process of the branching pattern to improve the transport properties of a vascular network. Recent studies show that part of endothelial cells (ECs) subjected to lower shear stress migrate toward vessels with higher shear stress in opposition to the blood flow for vessel regression. While dynamic changes of blood flow and local mechano-stress could coordinately modulate EC migration for vessel regression within the closed circulatory system, the effect of complexity of haemodynamic forces and vessel properties on vessel pruning remains elusive. Here, we reconstructed a 3-dimentsional (3D) vessel structure from 2D confocal images of the growing vessels in the mouse retina, and numerically obtained the local information of blood flow, shear stress and blood pressure in the vasculature. Moreover, we developed a predictive model for vessel pruning based on machine learning. We found that the combination of shear stress and blood pressure with vessel radius was tightly correlated to vessel pruning sites. Our results highlighted that orchestrated contribution of local haemodynamic parameters was important for the vessel pruning.

    DOI： 10.1371/journal.pcbi.1013565

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  • Cancer-associated fibroblast-derived SOD3 enhances lymphangiogenesis to drive metastasis in lung adenocarcinoma Reviewed International journal

    May Wathone Oo, Takao Hikita, Tomoha Mashima, Kosuke Torigata, Yin Min Thu, Tomohiro Habu, Hotaka Kawai, Toshiaki Ohara, Shuta Tomida, Sachio Ito, Ken Suzawa, Hitoshi Nagatsuka, Shinichi Toyooka, Masanori Nakayama

    Angiogenesis   28 ( 4 )   51 - 51   2025.9

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Abstract

    Despite advancements in diagnostic and therapeutic strategies, lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality due to its aggressive metastatic potential. Extracellular superoxide dismutase (SOD3) is an antioxidant enzyme that regulates oxidative stress and is regarded as a tumor suppressor. However, studies have demonstrated that SOD3 can either promote or inhibit cell proliferation and survival in various cancers, and its molecular mechanisms within the tumor microenvironment are poorly understood. In this study, we report a breakthrough in uncovering the role of SOD3 derived from cancer-associated fibroblasts (CAFs) in LUAD. Using LUAD xenograft models co-implanted with SOD3-overexpressing CAFs (CAFSOD3), we observe an aggressive tumor phenotype characterized by increased lymphangiogenesis and lymphatic vessel invasion (LVI) of the tumor. Additionally, LUAD patients with elevated SOD3 levels exhibit a higher incidence of LVI and metastasis. Notably, RNA sequencing of CAFSOD3 reveals that SOD3-mediated VEGF-dependent tumor progression and lymphangiogenesis are up-regulated. Furthermore, single-cell transcriptomic analysis of LUAD clinical samples confirms a strong correlation between SOD3 expression in fibroblasts and characteristics of tumor exacerbation, such as lymphangiogenesis and metastasis. These findings underscore new insights into the role of CAF-derived SOD3 in LUAD progression and highlight its potential as a biomarker and therapeutic target.

    DOI： 10.1007/s10456-025-10005-9

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    Other Link： https://link.springer.com/article/10.1007/s10456-025-10005-9/fulltext.html

  • Endothelial Cell Polarity in Health and Disease.

    Moe Thiha, Takao Hikita, Masanori Nakayama

    Acta medica Okayama   79 ( 1 )   1 - 7   2025.2

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    Endothelial cell polarity is fundamental to the organization and function of blood vessels, influencing processes such as angiogenesis, vascular stability, and response to shear stress. This review elaborates on the molecular mechanisms that regulate endothelial cell polarity, focusing on key players like the PAR polarity complex and Rho family GTPases. These pathways coordinate the front-rear, apical-basal and planar polarity of endothelial cells, which are essential for the proper formation and maintenance of vascular structures. In health, endothelial polarity ensures not only the orderly development of blood vessels, with tip cells adopting distinct polarities during angiogenesis, but also ensures proper vascular integrity and function. In disease states, however, disruptions in polarity contribute to pathologies such as coronary artery disease, where altered planar polarity exacerbates atherosclerosis, and cancer, where disrupted polarity in tumor vasculature leads to abnormal vessel growth and function. Understanding cell polarity and its disruption is fundamental not only to comprehending how cells interact with their microenvironment and organize themselves into complex, organ-specific tissues but also to developing novel, targeted, and therapeutic strategies for a range of diseases, from cardiovascular disorders to malignancies, ultimately improving patient outcomes.

    DOI： 10.18926/AMO/68353

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  • Early-stage antibody kinetics after the third dose of BNT162b2 mRNA COVID-19 vaccination measured by a point-of-care fingertip whole blood testing Reviewed

    Hideharu Hagiya, Yasuhiro Nakano, Masanori Furukawa, Naruhiko Sunada, Toru Hasegawa, Yasue Sakurada, Kou Hasegawa, Koichiro Yamamoto, Hiroko Ogawa, Takafumi Obara, Kouhei Ageta, Naomi Matsumoto, Rumi Matsuo, Tomoka Kadowaki, Akihito Higashikage, Takao Hikita, Takashi Yorifuji, Shinichi Toyooka, Yoshinobu Maeda, Yoshinori Yokokura, Fumio Otsuka, Masanori Nakayama

    Scientific Reports   12 ( 20628 )   2022.11

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    Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

    Abstract

    Amid the Coronavirus Disease 2019 pandemic, we aimed to demonstrate the accuracy of the fingertip whole blood sampling test (FWT) in measuring the antibody titer and uncovering its dynamics shortly after booster vaccination. Mokobio SARS-CoV-2 IgM & IgG Quantum Dot immunoassay (Mokobio Biotechnology R&D Center Inc., MD, USA) was used as a point-of-care FWT in 226 health care workers (HCWs) who had received two doses of the BNT162b2 mRNA vaccine (Pfizer-BioNTech) at least 8 months prior. Each participant tested their antibody titers before and after the third-dose booster up to 14-days. The effect of the booster was observed as early as the fourth day after vaccination, which exceeded the detection limit (> 30,000 U/mL) by 2.3% on the fifth day, 12.2% on the sixth day, and 22.5% after the seventh day. Significant positive correlations were observed between the pre- and post-vaccination (the seventh and eighth days) antibody titers (correlation coefficient, 0.405; p < 0.001). FWT is useful for examining antibody titers as a point-of-care test. Rapid response of antibody titer started as early as the fourth day post-vaccination, while the presence of weak responders to BNT162b2 vaccine was indicated.

    DOI： 10.1038/s41598-022-24464-3

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    Other Link： https://www.nature.com/articles/s41598-022-24464-3

  • Poor vaccine responsiveness towards third-dose mRNA vaccine of COVID-19 in Japanese older people Reviewed International journal

    Hideharu Hagiya, Takao Hikita, Tomohiro Habu, Masaki Asada, Takashi Yorifuji, Shinichi Toyooka, Fumio Otsuka, Masanori Nakayama

    Journal of Infection   85 ( 4 )   436 - 480   2022.7

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    DOI： 10.1016/j.jinf.2022.07.007

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  • Numerical evaluation reveals the effect of branching morphology on vessel transport properties during angiogenesis Reviewed International journal

    Fatemeh Mirzapour-Shafiyi, Yukinori Kametani, Takao Hikita, Yosuke Hasegawa, Masanori Nakayama

    PLoS Computational Biology   17 ( 6 )   e1008398   2021.6

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    Blood flow governs transport of oxygen and nutrients into tissues. Hypoxic tissues secrete VEGFs to promote angiogenesis during development and in tissue homeostasis. In contrast, tumors enhance pathologic angiogenesis during growth and metastasis, suggesting suppression of tumor angiogenesis could limit tumor growth. In line with these observations, various factors have been identified to control vessel formation in the last decades. However, their impacts on the vascular transport properties of oxygen remain elusive. Here, we take a computational approach to examine the effects of vascular branching on blood flow in the growing vasculature. First of all, we reconstruct a 3D vascular model from the 2D confocal images of the growing vasculature at postnatal day 5 (P5) mouse retina, then simulate blood flow in the vasculatures, which are obtained from the gene targeting mouse models causing hypo- or hyper-branching vascular formation. Interestingly, hyper-branching morphology attenuates effective blood flow at the angiogenic front, likely promoting tissue hypoxia. In contrast, vascular hypo-branching enhances blood supply at the angiogenic front of the growing vasculature. Oxygen supply by newly formed blood vessels improves local hypoxia and decreases VEGF expression at the angiogenic front during angiogenesis. Consistent with the simulation results indicating improved blood flow in the hypo-branching vasculature, VEGF expression around the angiogenic front is reduced in those mouse retinas. Conversely, VEGF expression is enhanced in the angiogenic front of hyper-branching vasculature. Our results indicate the importance of detailed flow analysis in evaluating the vascular transport properties of branching morphology of the blood vessels.

    DOI： 10.1371/journal.pcbi.1008398

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  • Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome. Reviewed International journal

    Mengnan Li, Shin-Ya Nishio, Chie Naruse, Meghan Riddell, Sabrina Sapski, Tatsuya Katsuno, Takao Hikita, Fatemeh Mizapourshafiyi, Fiona M Smith, Leanne T Cooper, Min Goo Lee, Masahide Asano, Thomas Boettger, Marcus Krueger, Astrid Wietelmann, Johannes Graumann, Bryan W Day, Andrew W Boyd, Stefan Offermanns, Shin-Ichiro Kitajiri, Shin-Ichi Usami, Masanori Nakayama

    Nature communications   11 ( 1 )   1343 - 1343   2020.3

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    Enlarged vestibular aqueduct (EVA) is one of the most commonly identified inner ear malformations in hearing loss patients including Pendred syndrome. While biallelic mutations of the SLC26A4 gene, encoding pendrin, causes non-syndromic hearing loss with EVA or Pendred syndrome, a considerable number of patients appear to carry mono-allelic mutation. This suggests faulty pendrin regulatory machinery results in hearing loss. Here we identify EPHA2 as another causative gene of Pendred syndrome with SLC26A4. EphA2 forms a protein complex with pendrin controlling pendrin localization, which is disrupted in some pathogenic forms of pendrin. Moreover, point mutations leading to amino acid substitution in the EPHA2 gene are identified from patients bearing mono-allelic mutation of SLC26A4. Ephrin-B2 binds to EphA2 triggering internalization with pendrin inducing EphA2 autophosphorylation weakly. The identified EphA2 mutants attenuate ephrin-B2- but not ephrin-A1-induced EphA2 internalization with pendrin. Our results uncover an unexpected role of the Eph/ephrin system in epithelial function.

    DOI： 10.1038/s41467-020-15198-9

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  • Regulation of programmed cell death ligand 1 expression by atypical protein kinase C lambda/iota in cutaneous angiosarcoma. Reviewed International journal

    Ai Kawamura, Takuji Kawamura, Meghan Riddell, Takao Hikita, Teruki Yanagi, Hiroshi Umemura, Masanori Nakayama

    Cancer science   110 ( 5 )   1780 - 1789   2019.5

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    The expression of immune checkpoint proteins such as programmed cell death protein 1 (PD-1) and its ligand (PD-L1) has been shown to correlate with patient prognosis in many malignant cancers. The expression of PD-L1 is controlled by c-Myc; however, further upstream regulation of PD-L1 expression is largely unknown. We have previously shown that atypical protein kinase C lambda/iota (aPKCλ) phosphorylates the Forkhead box protein O1 (FoxO1) transcription factor at Ser218 to suppress its DNA-binding ability, thereby regulating c-Myc expression and controlling physiologic and pathologic endothelial proliferation. The presence of phosphorylation of FoxO1 at Ser218 (pSer218 FoxO1) in cutaneous angiosarcoma (CAS) strongly correlates with poor patient prognosis. Here, we reported that patients with PD-L1+ cells in CAS lesions showed significantly worse prognosis compared to those that were PD-L1- . Expression of PD-L1 correlated with that of aPKCλ or the presence of pSer218FoxO1. Moreover, suppression of aPKCλ expression or inhibition of its activity in HUVECs or AS-M, an established human angiosarcoma cell line, resulted in decreased PD-L1 expression. Our results suggest that combined treatment with immune checkpoint inhibitors and aPKCλ inhibitors could be a novel treatment strategy for CAS patients.

    DOI： 10.1111/cas.13981

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  • aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability. Reviewed International journal

    Meghan Riddell, Akiko Nakayama, Takao Hikita, Fatemeh Mirzapourshafiyi, Takuji Kawamura, Ayesha Pasha, Mengnan Li, Mikio Masuzawa, Mario Looso, Tim Steinbacher, Klaus Ebnet, Michael Potente, Tomonori Hirose, Shigeo Ohno, Ingrid Fleming, Stefan Gattenlöhner, Phyu P Aung, Thuy Phung, Osamu Yamasaki, Teruki Yanagi, Hiroshi Umemura, Masanori Nakayama

    Nature communications   9 ( 1 )   5357 - 5357   2018.12

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    Strict regulation of proliferation is vital for development, whereas unregulated cell proliferation is a fundamental characteristic of cancer. The polarity protein atypical protein kinase C lambda/iota (aPKCλ) is associated with cell proliferation through unknown mechanisms. In endothelial cells, suppression of aPKCλ impairs proliferation despite hyperactivated mitogenic signaling. Here we show that aPKCλ phosphorylates the DNA binding domain of forkhead box O1 (FoxO1) transcription factor, a gatekeeper of endothelial growth. Although mitogenic signaling excludes FoxO1 from the nucleus, consequently increasing c-Myc abundance and proliferation, aPKCλ controls c-Myc expression via FoxO1/miR-34c signaling without affecting its localization. We find this pathway is strongly activated in the malignant vascular sarcoma, angiosarcoma, and aPKC inhibition reduces c-Myc expression and proliferation of angiosarcoma cells. Moreover, FoxO1 phosphorylation at Ser218 and aPKC expression correlates with poor patient prognosis. Our findings may provide a potential therapeutic strategy for treatment of malignant cancers, like angiosarcoma.

    DOI： 10.1038/s41467-018-07739-0

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  • PAR-3 controls endothelial planar polarity and vascular inflammation under laminar flow. Reviewed International journal

    Hikita T, Mirzapourshafiyi F, Barbacena P, Riddell M, Pasha A, Li M, Kawamura T, Brandes RP, Hirose T, Ohno S, Gerhardt H, Matsuda M, Franco CA, Nakayama M

    EMBO reports   19 ( 9 )   2018.9

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    Impaired cell polarity is a hallmark of diseased tissue. In the cardiovascular system, laminar blood flow induces endothelial planar cell polarity, represented by elongated cell shape and asymmetric distribution of intracellular organelles along the axis of blood flow. Disrupted endothelial planar polarity is considered to be pro-inflammatory, suggesting that the establishment of endothelial polarity elicits an anti-inflammatory response. However, a causative relationship between polarity and inflammatory responses has not been firmly established. Here, we find that a cell polarity protein, PAR-3, is an essential gatekeeper of GSK3β activity in response to laminar blood flow. We show that flow-induced spatial distribution of PAR-3/aPKCλ and aPKCλ/GSK3β complexes controls local GSK3β activity and thereby regulates endothelial planar polarity. The spatial information for GSK3β activation is essential for flow-dependent polarity to the flow axis, but is not necessary for flow-induced anti-inflammatory response. Our results shed light on a novel relationship between endothelial polarity and vascular homeostasis highlighting avenues for novel therapeutic strategies.

    DOI： 10.15252/embr.201745253

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  • Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell-cell Adhesion in the Postnatal Brain. Reviewed International journal

    Fujikake K, Sawada M, Hikita T, Seto Y, Kaneko N, Herranz-Pérez V, Dohi N, Homma N, Osaga S, Yanagawa Y, Akaike T, García-Verdugo JM, Hattori M, Sobue K, Sawamoto K

    The Journal of neuroscience : the official journal of the Society for Neuroscience   38 ( 19 )   4598 - 4609   2018.5

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    In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell-cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening and in vivo loss-of-function and gain-of-function experiments, we found that Fyn promotes somal disengagement from the chains and is involved in neuronal migration from the RMS into the granule cell layer of the OB. Fyn knockdown or Dab1 (disabled-1) deficiency caused p120-catenin to accumulate and adherens junction-like structures to be sustained at the contact sites between neuroblasts. Moreover, a Fyn and N-cadherin double-knockdown experiment indicated that Fyn regulates the N-cadherin-mediated cell adhesion between neuroblasts. These results suggest that the Fyn-mediated control of cell-cell adhesion is critical for the detachment of chain-forming neuroblasts in the postnatal OB.SIGNIFICANCE STATEMENT In the postnatal brain, newly born neurons (neuroblasts) migrate in chain-like cell aggregates toward their destination, where they are dissociated into individual cells and mature. The cellular and molecular mechanisms controlling the detachment of neuroblasts from chains are not understood. Here we show that Fyn, a nonreceptor tyrosine kinase, promotes the somal detachment of neuroblasts from chains, and that this regulation is critical for the efficient migration of neuroblasts to their destination. We further show that Fyn and Dab1 (disabled-1) decrease the cell-cell adhesion between chain-forming neuroblasts, which involves adherens junction-like structures. Our results suggest that Fyn-mediated regulation of the cell-cell adhesion of neuroblasts is critical for their detachment from chains in the postnatal brain.

    DOI： 10.1523/JNEUROSCI.1960-17.2018

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  • PlexinD1 signaling controls morphological changes and migration termination in newborn neurons. Reviewed International journal

    Masato Sawada, Nobuhiko Ohno, Mitsuyasu Kawaguchi, Shih-Hui Huang, Takao Hikita, Youmei Sakurai, Huy Bang Nguyen, Truc Quynh Thai, Yuri Ishido, Yutaka Yoshida, Hidehiko Nakagawa, Akiyoshi Uemura, Kazunobu Sawamoto

    The EMBO journal   37 ( 4 )   2018.2

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    Newborn neurons maintain a very simple, bipolar shape, while they migrate from their birthplace toward their destinations in the brain, where they differentiate into mature neurons with complex dendritic morphologies. Here, we report a mechanism by which the termination of neuronal migration is maintained in the postnatal olfactory bulb (OB). During neuronal deceleration in the OB, newborn neurons transiently extend a protrusion from the proximal part of their leading process in the resting phase, which we refer to as a filopodium-like lateral protrusion (FLP). The FLP formation is induced by PlexinD1 downregulation and local Rac1 activation, which coincide with microtubule reorganization and the pausing of somal translocation. The somal translocation of resting neurons is suppressed by microtubule polymerization within the FLP The timing of neuronal migration termination, controlled by Sema3E-PlexinD1-Rac1 signaling, influences the final positioning, dendritic patterns, and functions of the neurons in the OB These results suggest that PlexinD1 signaling controls FLP formation and the termination of neuronal migration through a precise control of microtubule dynamics.

    DOI： 10.15252/embj.201797404

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  • Disrupted-in-schizophrenia 1 regulates transport of ITPR1 mRNA for synaptic plasticity Reviewed

    Daisuke Tsuboi, Keisuke Kuroda, Motoki Tanaka, Takashi Namba, Yukihiko Iizuka, Shinichiro Taya, Tomoyasu Shinoda, Takao Hikita, Shinsuke Muraoka, Michiro Iizuka, Ai Nimura, Akira Mizoguchi, Nobuyuki Shiina, Masahiro Sokabe, Hideyuki Okano, Katsuhiko Mikoshiba, Kozo Kaibuchi

    NATURE NEUROSCIENCE   18 ( 5 )   698 - +   2015.5

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    DOI： 10.1038/nn.3984

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  • Speed control for neuronal migration in the postnatal brain by Gmip-mediated local inactivation of RhoA Reviewed

    Haruko Ota*, Takao Hikita*, Masato Sawada*, Tomoki Nishioka, Mami Matsumoto, Masayuki Komura, Akihisa Ohno, Yukiyo Kamiya, Takuya Miyamoto, Naoya Asai, Atsushi Enomoto, Masahide Takahashi, Kozo Kaibuchi, Kazuya Sobue, Kazunobu Sawamoto

    NATURE COMMUNICATIONS   5   4532   2014.7

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    DOI： 10.1038/ncomms5532

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  • Rac1-mediated indentation of resting neurons promotes the chain migration of new neurons in the rostral migratory stream of post- natal mouse brain Reviewed

    Takao Hikita, Akihisa Ohno, Masato Sawada, Haruko Ota, Kazunobu Sawamoto

    JOURNAL OF NEUROCHEMISTRY   128 ( 6 )   790 - 797   2014.3

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    DOI： 10.1111/jnc.12518

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  • Proteomic analysis of Girdin-interacting proteins in migrating new neurons in the postnatal mouse brain Reviewed

    Haruko Ota, Takao Hikita, Tomoki Nishioka, Mami Matsumoto, Jun Ito, Naoya Asai, Atsushi Enomoto, Masahide Takahashi, Kozo Kaibuchi, Kazuya Sobue, Kazunobu Sawamoto

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   442 ( 1-2 )   16 - 21   2013.12

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    DOI： 10.1016/j.bbrc.2013.10.126

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  • Growth factors released from gelatin hydrogel microspheres increase new neurons in the adult mouse brain. Reviewed

    Nakaguchi K, Jinnou H, Kaneko N, Sawada M, Hikita T, Saitoh S, Tabata Y, Sawamoto K

    Stem cells international   2012   915160   2012

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  • Growth factors released from gelatin hydrogel microspheres increase new neurons in the adult mouse brain Reviewed

    Kanako Nakaguchi, Hideo Jinnou, Naoko Kaneko, Masato Sawada, Takao Hikita, Shinji Saitoh, Yasuhiko Tabata, Kazunobu Sawamoto

    Stem Cells International   2012   915160   2012

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    DOI： 10.1155/2012/915160

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  • Girdin Is an Intrinsic Regulator of Neuroblast Chain Migration in the Rostral Migratory Stream of the Postnatal Brain Reviewed

    Yun Wang, Naoko Kaneko, Naoya Asai, Atsushi Enomoto, Mayu Isotani-Sakakibara, Takuya Kato, Masato Asai, Yoshiki Murakumo, Haruko Ota, Takao Hikita, Takashi Namba, Keisuke Kuroda, Kozo Kaibuchi, Guo-li Ming, Hongjun Song, Kazunobu Sawamoto, Masahide Takahashi

    JOURNAL OF NEUROSCIENCE   31 ( 22 )   8109 - 8122   2011.6

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    DOI： 10.1523/JNEUROSCI.1130-11.2011

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  • Promotion of neuronal migration towards the injured mouse cerebral cortex using sustained release of chemoattractant from gelatin hydrogel microspheres Reviewed

    Hiroshi Masuda, Naoko Kaneko, Eisuke Kako, Takao Hikita, Yasuhiko Tabata, Kazunobu Sawamoto

    NEUROSCIENCE RESEARCH   71   E338 - E339   2011

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    DOI： 10.1016/j.neures.2011.07.1484

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  • Immunohistochemical Study of Vesicle Monoamine Transporter 2 in the Hippocampal Region of Genetic Animal Model of Schizophrenia Reviewed

    Shuji Iritani, Hirotaka Sekiguchi, Chikako Habuchi, Takao Hikita, Shinichiro Taya, Kozo Kaibuchi, Norio Ozaki

    SYNAPSE   64 ( 12 )   948 - 953   2010.12

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    DOI： 10.1002/syn.20846

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  • Dysfunction of dopamine release in the prefrontal cortex of dysbindin deficient sandy mice: An in vivo microdialysis study Reviewed

    Taku Nagai, Yuko Kitahara, Anna Shiraki, Takao Hikita, Shinichiro Taya, Kozo Kaibuchi, Kiyofumi Yamada

    NEUROSCIENCE LETTERS   470 ( 2 )   134 - 138   2010.2

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    DOI： 10.1016/j.neulet.2009.12.071

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  • Proteomic analysis reveals novel binding partners of dysbindin, a schizophrenia-related protein Reviewed

    Takao Hikita, Shinichiro Taya, Yasutaka Fujino, Setsuko Taneichi-Kuroda, Kanae Ohta, Daisuke Tsuboi, Tomoyasu Shinoda, Keisuke Kuroda, Yusuke Funahashi, Junko Uraguchi-Asaki, Ryota Hashimoto, Kozo Kaibuchi

    JOURNAL OF NEUROCHEMISTRY   110 ( 5 )   1567 - 1574   2009.9

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    DOI： 10.1111/j.1471-4159.2009.06257.x

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  • Association analysis between schizophrenia and the AP-3 complex genes Reviewed

    Ryota Hashimoto, Kazutaka Ohi, Takeya Okada, Yuka Yasuda, Hidenaga Yamamori, Hiroaki Hori, Takao Hikita, Shinichiro Taya, Osamu Saitoh, Asako Kosuga, Masahiko Tatsumi, Kunitoshi Kamijima, Kozo Kaibuchi, Masatoshi Takeda, Hiroshi Kunugi

    NEUROSCIENCE RESEARCH   65 ( 1 )   113 - 115   2009.9

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    DOI： 10.1016/j.neures.2009.05.008

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  • Direct interaction of Dysbindin with the AP-3 complex via its mu subunit Reviewed

    Setsuko Taneichi-Kuroda, Shinichiro Taya, Takao Hikita, Yasutaka Fujino, Kozo Kaibuchi

    NEUROCHEMISTRY INTERNATIONAL   54 ( 7 )   431 - 438   2009.6

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    DOI： 10.1016/j.neuint.2009.01.014

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  • Identification of YWHAE, a gene encoding 14-3-3epsilon, as a possible susceptibility gene for schizophrenia Reviewed

    Masashi Ikeda*, Takao Hikita*, Shinichiro Taya*, Junko Uraguchi-Asaki, Kazuhito Toyo-oka, Anthony Wynshaw-Boris, Hiroshi Ujike, Toshiya Inada, Keizo Takao, Tsuyoshi Miyakawa, Norio Ozaki, Kozo Kaibuchi, Nakao Iwata

    HUMAN MOLECULAR GENETICS   17 ( 20 )   3212 - 3222   2008.10

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1093/hmg/ddn217

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  • Establishment of a tissue-specific RNAi system in C-elegans Reviewed

    Hiroshi Qadota, Makiko Inoue, Takao Hikita, Mathias Koeppen, Jeffrey D. Hardin, Mutsuki Arnano, Donald G. Moerman, Kozo Kaibuchi

    GENE   400 ( 1-2 )   166 - 173   2007.10

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

    DOI： 10.1016/j.gene.2007.06.020

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  • DISC1 regulates neurotrophin-induced axon elongation via interaction with Grb2 Reviewed

    Tomoyasu Shinoda, Shinichiro Taya, Daisuke Tsuboi, Takao Hikita, Reiko Matsuzawa, Setsuko Kuroda, Akihiro Iwamatsu, Kozo Kaibuchi

    JOURNAL OF NEUROSCIENCE   27 ( 1 )   4 - 14   2007.1

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    DOI： 10.1523/JNEUROSCI.3825-06.2007

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  • DISC1 regulates the transport of the NUDEL/LIS1/14-3-3 epsilon complex through Kinesin-1 Reviewed

    Shinichiro Taya, Tomoyasu Shinoda, Daisuke Tsuboi, Junko Asaki, Kumiko Nagai, Takao Hikita, Setsuko Kuroda, Keisuke Kuroda, Mariko Shimizu, Shinji Hirotsune, Akihiro Iwamatsu, Kozo Kaibuchi

    JOURNAL OF NEUROSCIENCE   27 ( 1 )   15 - 26   2007.1

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    DOI： 10.1523/JNEUROSCI.3826-06.2006

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  • Regulatory machinery of UNC-33Ce-CRMP localization in neurites during neuronal development in Caenorhabditis elegans Reviewed

    D Tsuboi, T Hikita, H Qadota, M Amano, K Kaibuchi

    JOURNAL OF NEUROCHEMISTRY   95 ( 6 )   1629 - 1641   2005.12

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    DOI： 10.1111/j.1471-4159.2005.03490.x

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  • Identification of a novel Cdc42 GEF that is localized to the PAT-3-mediated adhesive structure Reviewed

    T Hikita, H Qadota, D Tsuboi, S Taya, DG Moerman, K Kaibuchi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   335 ( 1 )   139 - 145   2005.9

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    DOI： 10.1016/j.bbrc.2005.07.068

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MISC

  • 【神経再生の最前線】内在性神経幹細胞を用いた神経再生

    松本 真実, 匹田 貴夫, 澤本 和延

    BIO Clinica   28 ( 13 )   1228 - 1232   2013.12

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  • 実験講座 培養脳スライスを用いた新生ニューロンのライブイメージング

    藤掛 数馬, 匹田 貴夫, 祖父江 和哉, 澤本 和延

    Surgery Frontier   20 ( 3 )   333 - 337   2013.9

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    Language：Japanese   Publisher：(株)メディカルレビュー社  

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  • 脳梗塞後の修復メカニズムと細胞治療 脳修復過程における内在性神経前駆細胞の移動

    藤掛 数馬, 匹田 貴夫, 祖父江 和哉, 澤本 和延

    脳循環代謝   24 ( Suppl. )   102 - 106   2013.8

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  • 増殖因子の徐放化による正常脳及び傷害脳における脳室下帯ニューロン新生の賦活化

    神農英雄, 澤田雅人, 中口加奈子, 金子奈穂子, 匹田貴夫, 齋藤伸治, 田畑泰彦, 澤本和延

    再生医療   12   2013

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  • 脳卒中の再生医療に向けて

    太田 晴子, 匹田 貴夫, 祖父江 和哉, 澤本 和延

    循環器内科   68 ( 4 )   393 - 397   2010.10

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  • 【組織幹細胞のあらたな発見とその臨床応用】成体の脳組織における神経幹細胞と再生医療

    匹田 貴夫, 澤本 和延

    医学のあゆみ   231 ( 11 )   1112 - 1116   2009.12

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  • 統合失調症関連蛋白質dysbindinの新規結合パートナーのプロテオーム解析による解明(Proteomic analysis reveals novel binding partners of dysbindin, a schizophrenia-related protein)

    匹田 貴夫, 田谷 真一郎, 藤野 泰孝, 橋本 亮太, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   61回   222 - 222   2009.5

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  • 新規統合失調症発症脆弱性候補因子としての14-3-3epsilonの同定

    匹田 貴夫, 池田 匡志, 田谷 真一郎, 岩田 仲生, 貝淵 弘三

    日本薬理学雑誌   133 ( 3 )   32P - 32P   2009.3

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  • 新規Dysbindin結合分子としてのAP-3複合体の同定(Identification of the AP-3 complex as a novel Dysbindin-interacting molecule)

    藤野 泰孝, 匹田 貴夫, 黒田 摂子, 田谷 真一郎, 貝淵 弘三

    神経化学   47 ( 2-3 )   228 - 228   2008.8

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  • 統合失調症脆弱性因子DISC1によるNUDEL複合体、Grb2の軸索への輸送制御

    匹田 貴夫, 田谷 真一郎, 篠田 友靖, 貝淵 弘三

    日本薬理学雑誌   130 ( 3 )   7P - 7P   2007.9

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  • 統合失調症末期海馬ニューロンにおけるDisrupted-In-Shizophrenia-1の役割(Roles of Disrupted-In-Schizophrenia-1 in the later stage of hippocampal neuron)

    坪井 大輔, 田谷 真一郎, 篠田 友靖, 匹田 貴夫, 黒田 摂子, 貝淵 弘三

    神経化学   44 ( 2-3 )   184 - 184   2005.8

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Awards

  • EMBO Short-Term Fellowships

    2015.1   The European Molecular Biology Organization  

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  • Mark A. Smith Prize

    2013.8   International Society for Neurochemistry   Rac1-mediated indentation of resting neurons, promotes the chain migration of new neurons in the rostral migratory stream of post-natal mouse brain

    Takao Hikita

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Research Projects

  • 樹状細胞の活性化を介した抗腫瘍免疫応答の増強による新規肺腺癌治療戦略の基礎的検討

    Grant number：24K12030  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    土生 智大, 匹田 貴夫, 冨田 秀太, 豊岡 伸一, 枝園 和彦, 山本 寛斉, 中山 雅敬, 諏澤 憲

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    Grant amount：\4550000 （ Direct expense: \3500000 、 Indirect expense：\1050000 ）

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  • Blood flow mediates adipose tissue inflammation via endothelial cells.

    Grant number：22K08125  2022.04 - 2025.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    匹田 貴夫

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    Grant amount：\4160000 （ Direct expense: \3200000 、 Indirect expense：\960000 ）

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  • ほ乳類成体脳における新生細胞の運命決定・移動・極性形成

    2011.04 - 2012.04

    二国間交流事業 フランスとの共同研究(INSERM) 

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\5000000

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  • Cell adhesion mechanism of migrating new neurons

    Grant number：23700385  2011 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    HIKITA Takao

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    Grant amount：\4420000 （ Direct expense: \3400000 、 Indirect expense：\1020000 ）

    New neurons migrating in the rostral migratory stream of postnatal brain shows specific fashion of collective cell migration, ‘chain migration’. To clarify a molecular mechanism that control chain migration, we searched for cell-cell adhesion molecules that is expressed in new neurons, and identified two adhesion molecules. By using inhibitors, we identified signaling pathway that regulates localization of the adhesion molecules in new neurons. Furthermore, by using FRET -based biosensors, we observed an activation of Rho family small GTPases in the cell-cell contact site of new neurons. Further studies will be performed to establish a method to control migration and direction of new neurons in vivo.

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Class subject in charge

  • Basic Cancer Microenvironment （2025academic year） special  - その他

  • Biochemistry （2025academic year） Concentration  - その他