hiroshi ueda

J-GLOBAL         Last updated: Sep 25, 2019 at 04:58
 
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Name
hiroshi ueda
Affiliation
Kyoto University
Section
Graduate School of Pharmaceutical Sciences
Research funding number
00145674
ORCID ID
0000-0002-8002-0137

Academic & Professional Experience

 
Apr 1981
 - 
Mar 1983
Faculty (Assistant), Department of Pharmacology, Yokohama City University School of Medicine
 
Apr 1983
 - 
Aug 1991
Faculty (Assistant), Department of Pharmacology, Kyoto University, Faculty of Pharmaceutical Sciences
 
Sep 1991
 - 
Mar 1996
Associate Professor,, Department of Pharmacology, Yokohama City University School of Medicine
 
Apr 1996
 - 
Mar 2019
Professor & Chairman, Pharmaceutical Sciences, Nagasaki University
 
Apr 2002
 - 
Mar 2019
Professor & Chairman,, Graduate School of, Nagasaki University
 
Apr 2019
   
 
Researcher, Department of Molecular Pharmacology, Kyoto University Graduate School of Pharmaceutical Sciences
 
Jun 2019
 - 
Today
Emeritus Professor, Nagasaki University
 

Awards & Honors

 
Apr 1985
Prize of Encouragement for Young Scientists from the Society for Japanese Pharmacology, The Society for Japanese Pharmacology
 
Mar 1989
Prize of Encouragement from the Society for Japanese Pharmaceutical Sciences, The Society for Japanese Pharmaceutical Sciences
 
Mar 2019
The Pharmaceutical Society of Japan Award 2019, The Pharmaceutical Society of Japan
 

Published Papers

 
Hiroshi Ueda, Hiroyuki Neyama, Jun Nagai, Yosuke Matsushita, Tamotsu Tsukahara, Ryoko Tsukahara
Pain   159 2170-2178   Nov 2018
We have previously demonstrated that lysophosphatidic acid (LPA) plays key roles in the initial mechanisms for neuropathic pain (NeuP) development. Here, we examined whether LPA receptor mechanisms and LPA production are related to the glial activ...
Fujita W, Yokote M, Gomes I, Gupta A, Ueda H, Devi LA
Molecular pharmacology      Oct 2018   [Refereed]
Hiroyuki Neyama, Hiroyuki Neyama, Yusuke Hamada, Ryoko Tsukahara, Minoru Narita, Kazuhiro Tsukamoto, Hiroshi Ueda
Peptides   107 10-16   Sep 2018
© 2018 Elsevier Inc. Kyotorphin is a unique biologically active neuropeptide (L-tyrosine-L-arginine), which is reported to have opioid-like analgesic actions through a release of Met-enkephalin from the brain slices. N-methyl-L-tyrosine-L-arginine...
Hiroshi Ueda, Hayato Matsunaga, Yosuke Matsushita, Shiori Maeda, Ryusei Iwamoto, Shigeyuki Yokoyama, Shigeyuki Yokoyama, Mikako Shirouzu, Mikako Shirouzu
Expert Opinion on Biological Therapy   18 89-94   May 2018
© 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group. Objectives: Prothymosin α (ProTα) was reported to inhibit the neuronal necrosis by facilitating the plasma membrane localization of endocytosed glucose transporter 1/4 through...
Sebok Kumar Halder, Hiroshi Ueda
Journal of Pharmacology and Experimental Therapeutics   365 27-36   Apr 2018
Copyright © 2018 by The American Society for Pharmacology and Experimental Therapeutics. High-mobility group box 1 (HMGB1) is increased in the cerebrospinal fluid (CSF) and serum during the early and late phases of brain ischemia and is known to c...
Tamotsu Tsukahara, Shuhei Yamagishi, Hiroyuki Neyama, Hiroshi Ueda
Peptides   101 60-68   Mar 2018
© 2017 Elsevier Inc. Kyotorphin (KTP; L-tyrosyl-L-arginine), an opioid-like analgesic discovered in the bovine brain, is potentially a neuromodulator because of its localization in synaptosomes, the existence of a specific KTP receptor, and the pr...
Ryoko Tsukahara, Shinji Yamamoto, Keisuke Yoshikawa, Mari Gotoh, Mari Gotoh, Tamotsu Tsukahara, Hiroyuki Neyama, Satoshi Ishii, Noriyuki Akahoshi, Keisuke Yanagida, Hayakazu Sumida, Masatake Araki, Kimi Araki, Ken ichi Yamamura, Kimiko Murakami-Murofushi, Hiroshi Ueda
Journal of Pharmacological Sciences   136 93-96   Feb 2018
© 2018 The Authors Lysophosphatidic acid (LPA) and LPA1 receptor signaling play a crucial role in the initiation of peripheral nerve injury-induced neuropathic pain through the alternation of pain-related genes/proteins expression and demyelinatio...
Association Between Polymorphisms in the Purinergic P2Y12 Receptor Gene and Severity of Both Cancer Pain and Postoperative Pain.
Sumitani M, Nishizawa D, Nagashima M, Ikeda K, Abe H, Kato R, Ueda H, Yamada Y; Japanese TR-Cancer Pain research group
Pain Med.   19(2) 348-354   Feb 2018   [Refereed]
Hiroshi Ueda, Keita Sasaki, Sebok Kumar Halder, Yuichi Deguchi, Keizo Takao, Keizo Takao, Tsuyoshi Miyakawa, Tsuyoshi Miyakawa, Atsushi Tajima
Journal of Neurochemistry   141 124-136   Apr 2017
© 2017 International Society for Neurochemistry Prothymosin alpha (ProTα) is expressed in various mammalian organs including the neuronal nuclei in the brain, and is involved in multiple functions, such as chromatin remodeling, transcriptional reg...
LPA1 receptor involvement in fibromyalgia-like pain induced by intermittent psychological stress, empathy.
Ueda H, Neyama H
Neurobiology of Pain   1 16-25   Apr 2017   [Refereed]
Nguyen Tien Huy, Nguyen Tien Huy, Nguyen Tien Huy, Pham Lan Chi, Pham Lan Chi, Jun Nagai, Jun Nagai, Tran Ngoc Dang, Tran Ngoc Dang, Evaristus Chibunna Mbanefo, Evaristus Chibunna Mbanefo, Evaristus Chibunna Mbanefo, Ali Mahmoud Ahmed, Nguyen Phuoc Long, Nguyen Phuoc Long, Le Thi Bich Thoa, Le Thi Bich Thoa, Le Phi Hung, Le Phi Hung, Afaf Titouna, Afaf Titouna, Kaeko Kamei, Hiroshi Ueda, Hiroshi Ueda, Kenji Hirayama, Kenji Hirayama
Antimicrobial Agents and Chemotherapy   61    Feb 2017
© 2017 American Society for Microbiology. All Rights Reserved. It is essential to continue the search for novel antimalarial drugs due to the current spread of resistance against artemisinin by Plasmodium falciparum parasites. In this study, we de...
Hiroshi Ueda, Jun ichi Kurita, Hiroyuki Neyama, Yuuka Hirao, Hiroyuki Kouji, Hiroyuki Kouji, Tadashi Mishina, Masaji Kasai, Hirofumi Nakano, Hirofumi Nakano, Atsushi Yoshimori, Yoshifumi Nishimura
Bioorganic and Medicinal Chemistry Letters   27 4705-4709   Jan 2017
© 2017 Elsevier Ltd The neuron-restrictive silencing factor NRSF/REST binds to neuron-restrictive silencing elements in neuronal genes and recruits corepressors such as mSin3 to inhibit epigenetically neuronal gene expression. Because dysregulatio...
Ryoko Tsukahara, Hiroshi Ueda
Journal of Pharmacological Sciences   132 162-165   Oct 2016
© 2016 The Authors Lysophosphatidic acid (LPA) initiates demyelination following peripheral nerve injury, which causes neuropathic pain. Our previous in vivo and ex vivo studies using mice have demonstrated that LPA-induced demyelination of spinal...
Shiori Maeda, Keita Sasaki, Sebok Kumar Halder, Wakako Fujita, Hiroshi Ueda
Journal of Pharmacological Sciences   132 100-104   Sep 2016
© 2016 The Authors Prothymosin alpha (ProTα) suppresses stress-induced necrosis of cultured cortical neurons. As neuroprotection alone could not explain the long-lasting protective actions against cerebral ischemia by ProTα, we further examined wh...
Oi Omotuyi, Oi Omotuyi, H. Ueda, H. Ueda
Molecular Simulation   42 874-881   Jul 2016
© 2015 Taylor & Francis. S100A13 is S100 family of EF-hand-containing calcium-binding protein involved in the secretion of some growth factors and pro-inflammatory cytokines lacking signal peptides. The involvement of S100A13 in cancer progressi...
Takehiro Mukae, Wakako Fujita, Hiroshi Ueda
Journal of Pharmacological Sciences   131 64-67   May 2016
© 2016 The Authors. Pregabalin (PGB) is a valuable therapeutic drug against chronic pain. Here we attempted to perform the combinatorial drug therapy with P-glycoprotein (P-gp) inhibitors to lower therapeutic dosage of PGB in the intermittent cold...
H. Ueda, S. K. Halder, H. Matsunaga, K. Sasaki, S. Maeda
Neuroscience   318 206-218   Mar 2016
© 2016 IBRO.Published by Elsevier Ltd. Prothymosin alpha (ProTα) has robustness roles against brain and retinal ischemia or serum-starvation stress. In the ProTα sequence, the active core 30-amino acid peptide/P30(a.a.49-78) is necessary for the o...
Caroline Mwendwa Kijogi, Caroline Mwendwa Kijogi, Christopher Khayeka-Wandabwa, Christopher Khayeka-Wandabwa, Keita Sasaki, Yoshimasa Tanaka, Hiroshi Kurosu, Hayato Matsunaga, Hiroshi Ueda
BMC Physiology   16    Mar 2016
© 2016 Kijogi et al. Background: The cell type, cell status and specific localization of Prothymosin α (PTMA) within cells seemingly determine its function. PTMA undergoes 2 types of protease proteolytic modifications that are useful in elucidatin...
Masahiko Sumitani, Hiroshi Ueda, Jun Hozumi, Reo Inoue, Takamichi Kogure, Takamichi Kogure, Yoshitsugu Yamada
Journal of Pain and Palliative Care Pharmacotherapy   30 31-35   Jan 2016
© 2016 Taylor and Francis Group, LLC. Recent understanding of the neuron-glia communication shed light on an important role of microglia to develop neuropathic pain The analgesic effect of minocycline on neuropathic pain is promising but it remain...
Keita Sasaki, Olaposi Idowu Omotuyi, Mutsumi Ueda, Kazuyuki Shinohara, Hiroshi Ueda
Molecular Brain   8    Dec 2015
© 2015 Sasaki et al. Background: Structural and functional changes of the hippocampus are correlated with psychiatric disorders and cognitive dysfunctions. Genetic deletion of heparin-binding epidermal growth factor-like growth factor (HB-EGF), wh...
Sebok Kumar Halder, Hayato Matsunaga, Ken J. Ishii, Hiroshi Ueda
Journal of Neurochemistry   135 1161-1177   Dec 2015
© 2015 International Society for Neurochemistry. Prothymosin-alpha protects the brain and retina from ischemic damage. Although prothymosin-alpha contributes to toll-like receptor (TLR4)-mediated immnunopotentiation against viral infection, the be...
Keqiang Xie, Ikuo Masuho, Chien Cheng Shih, Chien Cheng Shih, Yan Cao, Keita Sasaki, Chun Wan J. Lai, Pyung Lim Han, Hiroshi Ueda, Carmen W. Dessauer, Michelle E. Ehrlich, Michelle E. Ehrlich, Michelle E. Ehrlich, Baoji Xu, Barry M. Willardson, Kirill A. Martemyanov
eLife   4 1-21   Nov 2015
© Xie et al. In the striatum, signaling via G protein-coupled neurotransmitter receptors is essential for motor control. Critical to this process is the effector enzyme adenylyl cyclase type 5 (AC5) that produces second messenger cAMP upon recepto...
Hitoshi Uchida, Yosuke Matsushita, Kohei Araki, Takehiro Mukae, Hiroshi Ueda
Journal of Pharmacological Sciences   128 208-211   Sep 2015
© 2015 The Authors Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. Neuropathic pain is often insensitive to morphine. Our previous study has demonstrated that neuron-restrictive silencer factor represses mu o...
Olaposi I. Omotuyi, Olaposi I. Omotuyi, Jun Nagai, Hiroshi Ueda, Hiroshi Ueda
Scientific Reports   5    Aug 2015
Lysophosphatidic acid (LPA) receptor 1 (LPA 1) is a member of the G protein-coupled receptors mediating the biological response to LPA species. Lack of detailed mechanism underlying LPA/LPA 1 interaction has hampered the development of specific an...
Takehiro Mukae, Hitoshi Uchida, Hiroshi Ueda
Journal of Pharmacology and Experimental Therapeutics   353 471-479   Jun 2015
Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics. Treatment of fibromyalgia is an unmet medical need. To develop novel therapies for the treatment of fibromyalgia, we explored pain therapeutic actions of exis...
Nan Jia, Nan Jia, Nan Jia, Yuka Nakazawa, Yuka Nakazawa, Chaowan Guo, Chaowan Guo, Mayuko Shimada, Mayuko Shimada, Mieran Sethi, Yoshito Takahashi, Yoshito Takahashi, Hiroshi Ueda, Yuji Nagayama, Tomoo Ogi, Tomoo Ogi, Tomoo Ogi
Nature Protocols   10 12-24   Jan 2015
© 2014 Nature America, Inc. All rights reserved. DNA repair systems protect cells from genomic instability and carcinogenesis. Therefore, assays for measuring DNA repair activity are valuable, not only for clinical diagnoses of DNA repair deficien...
Olaposi Omotuyi, Hayato Matsunaga, Hiroshi Ueda
Expert Opinion on Biological Therapy   15 223-229   Jan 2015
© 2015 Informa UK, Ltd. Objective: During preconditioning, lipopolysaccharide (LPS) selectively activates TLR4/MD-2/Toll/IL-1 receptor-domain-containing adaptor inducing IFN-b (TRIF) pathway instead of pro-inflammatory myeloid differentiation prot...
Hiroshi Ueda, Hitoshi Uchida
Current Pharmaceutical Design   21 849-867   Jan 2015
© 2015 Bentham Science Publishers. Neuropathic pain is characterized by complicated combination of positive (e.g., hyperalgesia and allodynia) and negative (e.g., hypoesthesia and hypoalgesia) symptoms, and is often refractory to conventional phar...
Olaposi I. Omotuyi, Olaposi I. Omotuyi, Hiroshi Ueda, Hiroshi Ueda
Computational Biology and Chemistry   55 14-22   Jan 2015
© 2015 Elsevier Ltd. All rights reserved. Plastic changes in the brain required for memory formation and long-term learning are dependent on N-methyl-d-aspartic acid (NMDA) receptor signaling. Nefiracetam reportedly boosts NMDA receptor functions ...
Flaminia Pavone, Hiroshi Ueda
Pain   155 649-650   Jan 2014
Hitoshi Uchida, Jun Nagai, Hiroshi Ueda
Molecular pain   10 71   Jan 2014
BACKGROUND: Paclitaxel, which is widely used for the treatment of solid tumors, causes neuropathic pain via poorly understood mechanisms. Previously, we have demonstrated that lysophosphatidic acid (LPA) and its receptors (LPA1 and LPA3) are requi...
Descriptor-based Fitting of LPA3 Antagonists into a Single Predictive Mathematical Model.
Omotuyi OI, Ueda H
Biomath   3(1406131) 1-7   Jan 2014   [Refereed]
Yosuke Matsushita, Idowu O. Omotuyi, Takehiro Mukae, Hiroshi Ueda
Current Pharmaceutical Design   19 7355-7361   Dec 2013
Herein, we investigated the role of periaqueductal gray (PAG)-resident microglia in the development of morphine tolerance and its underlying mechanisms. We showed that clodronate and minocycline known as microglia inhibitors reversed morphine tole...
Yosuke Matsushita, Kohei Araki, Olaposi Idowu Omotuyi, Takehiro Mukae, Hiroshi Ueda
British Journal of Pharmacology   170 991-998   Nov 2013
Background and Purpose Hypoesthesia is a clinical feature of neuropathic pain. The feature is partly explained by the evidence of epigenetic repression of Nav1.8 sodium channel in the dorsal root ganglion (DRG). Experimental Approach We investigat...
Ryo Yano, Lin Ma, Jun Nagai, Hiroshi Ueda
Cellular and Molecular Neurobiology   33 1033-1041   Aug 2013
Lysophosphatidic acid (LPA) is a bioactive lipid mediator that exerts a wide range of biological actions. In recent decades, LPA has been demonstrated as an important initiator of neuropathic pain based on the mechanisms of LPA-induced feed-forwar...
Yoshishige Miyabe, Chie Miyabe, Chie Miyabe, Yoshiko Iwai, Aiko Takayasu, Shin Fukuda, Waka Yokoyama, Jun Nagai, Masahiro Jona, Yasunori Tokuhara, Ryunosuke Ohkawa, Harald M. Albers, Huib Ovaa, Junken Aoki, Jerold Chun, Yutaka Yatomi, Hiroshi Ueda, Masayuki Miyasaka, Nobuyuki Miyasaka, Toshihiro Nanki
Arthritis and Rheumatism   65 2037-2047   Aug 2013
Objective Lysophosphatidic acid (LPA) is a bioactive lipid that binds to a group of cell surface G protein-coupled receptors (LPA receptors 1-6 [LPA 1-6]) and has been implicated as an important mediator of angiogenesis, inflammation, and cancer g...
Sebok K. Halder, Hayato Matsunaga, Ken J. Ishii, Shizuo Akira, Kensuke Miyake, Hiroshi Ueda
Journal of Neurochemistry   126 243-260   Jul 2013
Reprogramming of toll-like receptor 4 (TLR4) by brief ischemia or lipopolysacharide (LPS) contributes to superintending tolerance against destructive ischemia in brain. However, beneficial roles of TLR4 signaling in ischemic retina are not well kn...
Descriptor-based Fitting of Structurally Diverse LPA1 Inhibitors into a Single predictive Mathematical Model.
Omotuyi OI, Ueda H
Journal of Physical Chemistry & Biophysics   3(3)    Jul 2013   [Refereed]
Lin Ma, Jun Nagai, Jerold Chun, Hiroshi Ueda
Molecular Pain   9    Jun 2013
Background: We previously reported that nerve injury-induced neuropathic pain is initiated by newly produced lysophosphatidic acid (LPA).Results: In this study, we developed a quantitative mass spectrometry for detecting LPA species by using Phos-...
H. Uchida, H. Uchida, Y. Matsushita, H. Ueda
Neuroscience   240 147-154   Jun 2013
Brain-derived neurotrophic factor (BDNF) is known to be up-regulated in the dorsal root ganglion (DRG) after peripheral nerve injury, and to contribute to neuropathic pain. Here, we found that thermal hyperalgesia and mechanical allodynia at day 7...
Sebok Kumar Halder, Hayato Matsunaga, Haruka Yamaguchi, Hiroshi Ueda
Journal of Neurochemistry   125 713-723   Jun 2013
Prothymosin alpha (ProTα), a nuclear protein, is implicated in the inhibition of ischemia-induced necrosis as well as apoptosis in the brain and retina. Although ProTα has multiple biological functions through distinct regions in its sequence, it ...
Sebok Kumar Halder, Junya Sugimoto, Hayato Matsunaga, Hiroshi Ueda
Peptides   43 68-75   May 2013
Prothymosin alpha (ProTα), a nuclear protein, plays multiple functions including cell survival. Most recently, we demonstrated that the active 30-amino acid peptide sequence/P30(amino acids 49-78) in ProTα retains its substantial activity in neuro...
S. K. Halder, R. Yano, J. Chun, H. Ueda
Neuroscience   235 10-15   Apr 2013
We demonstrated previously that the lysophosphatidic acid-1 (LPA1) receptor plays a crucial role in the initiation of peripheral nerve injury-induced neuropathic pain through the alternation of pain-related genes/proteins expression and demyelinat...
Keita Sasaki, Tatsuro Yamasaki, Idowu O. Omotuyi, Masayoshi Mishina, Hiroshi Ueda
Journal of Neurochemistry   124 844-854   Mar 2013
Gγ7 is enriched in striatum and forms a heterotrimeric complex with Gαolf/Gβ, which is coupled to D1 receptor (D1R). Here, we attempted to characterize the pathophysiological, neurochemical, and pharmacological features of mice deficient of Gγ7 ge...
Hiroshi Ueda
Lysophospholipid Receptors: Signaling and Biochemistry   433-449   Feb 2013
Olaposi I. Omotuyi, Hiroshi Ueda
Current Bioinformatics   8 603-610   Jan 2013
G-protein-coupled receptors (GPCRs) mediate diverse biological functions through intracellular signal cascades initiated by intracellular G-protein coupling following extracellular agonist binding. GPCRs are quintessential targets for drug design ...
Sebok Kumar Halder, Hayato Matsunaga, Hiroshi Ueda
Journal of Neurochemistry   123 262-275   Nov 2012
Prothymosin alpha (ProTα), a nuclear protein devoid of signal sequence, has been shown to possess a number of cellular functions including cell survival. Most recently, we demonstrated that ProTα is localized in the nuclei of neurons, while it is ...
Lin Ma, Jun Nagai, Yuki Sekino, Yoshitaka Goto, Shinji Nakahira, Hiroshi Ueda
Journal of Pharmacological Sciences   119 282-286   Aug 2012
Botulinum toxin type A is a unique candidate for inhibition of pain transmission. In the present study we attempted to see the beneficial actions of A2 neurotoxin (NTX), an active subunit of botulinum toxin type A. Intraplantar injection of A2 NTX...
Sebok Kumar Halder, Hiroshi Ueda
Cellular and Molecular Neurobiology   32 59-66   Jan 2012
Prothymosin alpha (ProTα) is an acidic nuclear protein implicated in several cellular functions including cell survival. ProTα is found in the central nervous system, but the regional and cell type-specific expression patterns are not known. In th...
Hiroshi Ueda, Hayato Matsunaga, Sebok Kumar Halder
Annals of the New York Academy of Sciences   1269 34-43   Jan 2012
Prothymosin α (ProTα) possesses multiple functions for cell robustness. This protein functions intracellularly to stimulate cell proliferation and differentiation through epigenetic or genomic mechanisms. ProTα also regulates the cell defensive me...
Michiko Nishiyori, Hitoshi Uchida, Jun Nagai, Kohei Araki, Takehiro Mukae, Shiroh Kishioka, Hiroshi Ueda
Molecular Pain   7    Sep 2011
Background: Fibromyalgia (FM) is characterized by chronic widespread pain, which is often refractory to conventional painkillers. Numerous clinical studies have demonstrated that antidepressants are effective in treating FM pain. We previously est...
Hiroshi Ueda
Biological and Pharmaceutical Bulletin   34 1154-1158   Aug 2011
The injury-induced intense stimulation of spinal cord neurons causes lysophosphatidic acid (LPA) biosynthesis. LPA1 receptor activation causes demyelination and sprouting of dorsal root fibers, leading to an induction of synaptic reorganization un...
Jun Nagai, Hiroshi Ueda
Journal of Neurochemistry   118 256-265   Jul 2011
We have previously demonstrated that lysophosphatidic acid (LPA) production in the spinal cord following partial sciatic nerve injury (SCNI) and its signaling initiate neuropathic pain. In order to examine whether LPA production depends on the int...
Yasutaka Kakiuchi, Jun Nagai, Mari Gotoh, Harumi Hotta, Hiromu Murofushi, Tomoyo Ogawa, Hiroshi Ueda, Kimiko Murakami-Murofushi
Molecular Pain   7    May 2011
Background: Cyclic phosphatidic acid (cPA) is a structural analog of lysophosphatidic acid (LPA), but possesses different biological functions, such as the inhibition of autotaxin (ATX), an LPA-synthesizing enzyme. As LPA is a signaling molecule i...
Hiroshi Ueda, Mutsumi Ueda
Clinical Lipidology   6 147-158   Apr 2011
The injury-induced intense stimulation of spinal cord neurons causes lysophosphatidic acid (LPA) synthesis. LPA1receptor activation causes demyelination and sprouting of sensory fibers, leading to an induction of synaptic reorganization underlying...
Jun Nagai, Hitoshi Uchida, Yosuke Matsushita, Ryo yano, Mutsumi Ueda, Masami Niwa, Junken Aoki, Jerold Chun, Hiroshi Ueda
Molecular Pain   6    Nov 2010
Background: Although neuropathic pain is frequently observed in demyelinating diseases such as Guillain-Barré syndrome and multiple sclerosis, the molecular basis for the relationship between demyelination and neuropathic pain behaviors is poorly ...
H. Matsunaga, H. Matsunaga, H. Ueda
Cell Death and Differentiation   17 1760-1772   Nov 2010
The nuclear protein prothymosin-α (ProTα), which lacks a signal peptide sequence, is released from neurons and astrocytes on ischemic stress and exerts a unique form of neuroprotection through an anti-necrotic mechanism. Ischemic stress-induced Pr...
Lin Ma, Jun Nagai, Hiroshi Ueda
Journal of Neurochemistry   115 643-653   Nov 2010
We recently demonstrated that de novo lysophosphatidic acid (LPA) production in the spinal cord occurs in the early phase after nerve injury or LPA injection, and underlies the peripheral mechanisms of neuropathic pain. In this study, we examined ...
Hayato Matsunaga, Hayato Matsunaga, Kaori Mizota, Hitoshi Uchida, Takafumi Uchida, Hiroshi Ueda
Journal of Neurochemistry   114 1333-1343   Sep 2010
The present study demonstrates a novel high-affinity neuronal target for endocrine disrupting chemicals (EDCs), which potentially cause psychological disorders. EDCs competitively inhibited the binding of bovine serum albumin-conjugated progestero...
Ma L, Uchida H, Nagai J, Inoue M, Aoki J, Ueda H
The Journal of pharmacology and experimental therapeutics   333(2) 540-546   May 2010   [Refereed]
H. Uchida, K. Sasaki, L. Ma, H. Ueda
Neuroscience   166 1-4   Mar 2010
Peripheral nerve injury causes a variety of alterations in pain-related gene expression in primary afferent, which underlie the neuronal plasticity in neuropathic pain. One of the characteristic alterations is a long-lasting downregulation of volt...
Uchida H, Ma L, Ueda H
The Journal of neuroscience : the official journal of the Society for Neuroscience   30(13) 4806-4814   Mar 2010   [Refereed]
Nishiyori M, Nagai J, Nakazawa T, Ueda H
Neuroscience letters   472(3) 184-187   Mar 2010   [Refereed]
Xie W, Uchida H, Nagai J, Ueda M, Chun J, Ueda H
Journal of neurochemistry   113(4) 1002-1011   Mar 2010   [Refereed]
Hiroshi Ueda, Hayato Matsunaga, Hitoshi Uchida, Mutsumi Ueda
Annals of the New York Academy of Sciences   1194 20-26   Jan 2010
Following stroke or traumatic damage, neuronal death via both necrosis and apoptosis causes loss of functions, including memory, sensory perception, and motor skills. As necrosis has the nature to expand, while apoptosis stops the cell death casca...
Matsumoto M, Kondo S, Usdin TB, Ueda H
Journal of neurochemistry   112(2) 521-530   Jan 2010   [Refereed]
Ma L, Uchida H, Nagai J, Inoue M, Chun J, Aoki J, Ueda H
Molecular pain   5 64   Nov 2009   [Refereed]
Ueda H, Ueda M
Frontiers in bioscience : a journal and virtual library   14 5260-5272   Jun 2009   [Refereed]
Matsushita Y, Ueda H
Neuroreport   20 63-68   Jan 2009   [Refereed]
R. Fujita, M. Ueda, K. Fujiwara, H. Ueda
Cell Death and Differentiation   16 349-358   Jan 2009
Prothymosin-α (ProTα) causes a switch in cell death mode from necrosis to neurotrophin-reversible apoptosis in primary cultured cortical neurons. In the present study, post-ischemic administration (3 or 24h, intravenously) of recombinant mouse Pro...
Inoue M, Ma L, Aoki J, Ueda H
Journal of neurochemistry   107(6) 1556-1565   Dec 2008   [Refereed]
Nishiyori M, Ueda H
Molecular pain   4 52   Nov 2008   [Refereed]
Mizota K, Ueda H
Neuroreport   19 1529-1533   Oct 2008   [Refereed]
Matsumoto M, Xie W, Ma L, Ueda H
Molecular pain   4 25   Jul 2008   [Refereed]
Ueda H
Naunyn-Schmiedeberg's archives of pharmacology   377 315-323   Jun 2008   [Refereed]
M. Inoue, W. Xie, Y. Matsushita, J. Chun, J. Aoki, H. Ueda
Neuroscience   152 296-298   Mar 2008
Lysophosphatidic acid receptor (LPA1) signaling initiates neuropathic pain and several pathological events in a partial sciatic nerve injury model. Recently, we reported that lysophosphatidic acid (LPA) induces neuropathic pain as well as demyelin...
Inoue M, Ma L, Aoki J, Chun J, Ueda H
Molecular pain   4 6   Feb 2008   [Refereed]
Matsumoto M, Xie W, Inoue M, Ueda H
Molecular pain   3 41   Dec 2007   [Refereed]
R. Fujita, H. Ueda
Cell Death and Differentiation   14 1839-1842   Oct 2007
Nagai J, Kurokawa M, Takeshima H, Kieffer BL, Ueda H
The Journal of pharmacology and experimental therapeutics   321 195-201   Apr 2007   [Refereed]
Ueda H, Fujita R, Yoshida A, Matsunaga H, Ueda M
The Journal of cell biology   176(6) 853-862   Mar 2007   [Refereed]
Fujita R, Kiguchi N, Ueda H
Neurochemistry international   50 351-355   Jan 2007   [Refereed]
Md Harunor Rashid, Md Harunor Rashid, Hidemasa Furue, Megumu Yoshimura, Hiroshi Ueda
Pain   125 125-135   Nov 2006
In the spinal dorsal horn, activation of the nicotinic acetylcholine receptors (nAChR) by exogenously applied agonists is known to enhance inhibitory synaptic transmission, and to produce analgesia. However, it is still unknown whether endogenousl...
Inoue M, Yamaguchi A, Kawakami M, Chun J, Ueda H
Molecular pain   2 25   Aug 2006   [Refereed]
Matsunaga H, Ueda H
Neurochemistry international   49 294-303   Aug 2006   [Refereed]
Matsumoto M, Inoue M, Hald A, Xie W, Ueda H
The Journal of pharmacology and experimental therapeutics   318 735-740   Aug 2006   [Refereed]
Matsunaga H, Ueda H
Cellular and molecular neurobiology   26 237-246   May 2006   [Refereed]
Matsumoto M, Inoue M, Ueda H
Neuroscience letters   397 249-253   Apr 2006   [Refereed]
Mizota K, Ueda H
Toxicological sciences : an official journal of the Society of Toxicology   90 362-368   Apr 2006   [Refereed]
Yue Li, Yumiko Saito, Masahiko Suzuki, Hiroshi Ueda, Makoto Endo, Kei Maruyama
Biochemical and Biophysical Research Communications   339 805-809   Jan 2006
Several endogenous peptides for G-protein-coupled receptors have been found to play physiological roles in muscle contraction in addition to their well-demonstrated actions in other tissues. To further identify such peptides, we screened over 400 ...
Ueda H
Pharmacology & therapeutics   109 57-77   Jan 2006   [Refereed]

Misc

 
植田弘師
医学のあゆみ   264(12) 1016‐1019   Mar 2018
Hiroshi Ueda, Shiori Maeda
Folia Pharmacologica Japonica   151(1) 15-19   Jan 2018
© 2018, Japanese Pharmacological Society. All rights reserved. Prothymosin alpha (ProTα) has been identified as an anti-necrotic factor from the conditioned medium of primary cultured of rat cortical neurons under the serum-free starving condition...
Hiroshi Ueda, Hitoshi Uchida
Bioactive Lipid Mediators: Current Reviews and Protocols   223-236   Jan 2015
© Springer Japan 2015. Chronic pain is considered to have a memory process because of its longlasting nature even after the original cause such as nerve injury is resolved. This type contrasts to the cases with acute pain, nociceptive or inflammat...
【疼痛研究の新展開:基礎研究者の視点】 痛みによるepigenetic修飾
植田 弘師, 内田 仁司
脳21   17(2) 161-165   Apr 2014
末梢神経の損傷は、陽性症状(疼痛過敏やアロディニア)と陰性症状(知覚鈍麻)が混在する慢性疼痛(神経障害性疼痛)を誘発する。その病態メカニズムにおいて、遺伝子発現変調を介する痛み伝達経路の機能的異常が重要な役割を果たすと考えられてきた。最近の研究から、クロマチン構造の再構築を介して遺伝子発現を制御するエピジェネティクス修飾が、神経障害性疼痛の発症維持に関与することが明らかになりつつある。本稿では、神経障害性疼痛に対するエピジェネティクス治療の有用性を含めて、著者らの報告を中心に概説する。(著...
【研究成果を薬につなげるアカデミア創薬の戦略と実例】 (第2章)アカデミア創薬研究の今を知る 《各疾患領域におけるニーズと研究戦略》 神経疾患領域におけるアカデミア創薬
植田 弘師, 松永 隼人
実験医学   32(2) 336-342   Feb 2014
神経疾患は、アンメットメディカルニーズ(未充足の医療ニーズ)の高い領域であり、市場の成長性が見込まれることから多くの企業が開発の重点領域に掲げている。世界の医薬品市場における疾患負荷の約35%を占めることからも、今後、革新的な神経疾患治療法、治療薬の需要が拡大されることは想像に難くない。本稿では、長崎大学創薬拠点における特徴ある創薬研究の取り組みと、本拠点で遂行している神経疾患創薬の脳梗塞治療薬と慢性疼痛治療薬の取り組みを紹介する。(著者抄録)
【最新生理活性脂質研究-実験手法、基礎的知識とその応用-】 (第4章)臨床編 慢性疼痛創薬標的としてのリゾホスファチジン酸
植田 弘師, 永井 潤
遺伝子医学MOOK   (24) 260-266   May 2013
脂質メディエーターが痛みの制御因子であることは古くから知られており,炎症性疼痛メディエーターとしてのプロスタノイド,鎮痛メディエーターとしてのカンナビノイドに加え,慢性疼痛メディエーターとしてのリゾホスファチジン酸(LPA)が構成因子である。昨今ではLPAは慢性炎症にも関与する可能性が報告され,幅広く慢性疾患原因分子としての役割が確立しつつあり,同時に創薬標的として注目されている。本稿では,慢性疼痛時のLPAの合成や作用機構に着目し,その最近の研究成果を紹介する。(著者抄録)
Hiroshi Ueda, Hayato Matsunaga, Omotuyi I. Olaposi, Jun Nagai
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids   1831 61-73   Jan 2013
Acute inflammatory pain signal originates from transient hypersensitivity in afferent fibers when depolarized via injured tissues or proinflammatory cells-derived pronociceptive ligand binding. This pain is sensitive to opioids and NSAIDs. In neur...
神経障害性疼痛における生理活性脂質LPAの生合成機構および病態機能
植田 弘師, 永井 潤
ペインクリニック   33(11) 1575-1583   Nov 2012
わが国においても神経障害性疼痛の治療薬としてプレガバリンが承認され、既に一定の治療効果が得られている。しかしながら、高用量または長期投与による副作用の問題、あるいは複雑な疼痛病態のため、必ずしもこれらの疼痛治療薬が著効しない症例などが存在する。今後、創薬の観点から求められる神経障害性疼痛の基礎研究は、慢性疼痛病態特異的かつ共通する分子メカニズムの解明である。われわれは、神経障害性疼痛原因分子リゾホスファチジン酸(LPA)に着目して、神経障害性疼痛の基盤解明に取り組んできており、最近では新規...
【線維筋痛症治療の発展】 [第2部]線維筋痛症の薬物療法
西依 倫子, 植田 弘師
難病と在宅ケア   17(6) 38-42   Sep 2011
神経障害性疼痛を担うフィードフォワード増幅機構
植田 弘師, 内田 仁司
ペインクリニック   30(11) 1539-1544   Nov 2009
神経損傷により誘導される慢性疼痛は、抗炎症薬やモルヒネによって除痛されにくいことから難治性神経障害性疼痛と呼ばれている。筆者らは近年、神経損傷後、長期に認められる痛覚過敏とアロディニア現象を誘導する初発因子として、脂質メディエーターであるリゾホスファチジン酸を同定した。この分子は、強度の侵害刺激に応じて産生され、神経障害性疼痛の分子基盤となる疼痛関連分子の発現変調や脱髄現象を誘発する。さらにこの分子はグリア細胞を活性化し、これらがフィードフォワード増幅機構として痛みの慢性化につながる可能性...
[Anti-opioid action of glutamate-NMDA receptor systems underlying morphine analgesic tolerance]
Ueda H, Matsushita Y
Masui. The Japanese journal of anesthesiology   58 1136-1142   Sep 2009   [Refereed]
【神経障害性疼痛の基礎と臨床】 神経障害性疼痛に関する基礎研究 リゾホスファチジン酸誘発性神経障害性疼痛
植田 弘師, 永井 潤
ペインクリニック   30(別冊春) S81-S86   Apr 2009
著者らは、神経障害性疼痛の初発因子として脂質メディエーターであるリゾホスファチジン酸(LPA)を同定した。本稿では、LPAが引き起こす疼痛過敏・アロディニア現象について、知覚神経の脱髄とそれに伴うエファプス/スプラウティングといった可塑的変化やCa2+チャネルなどの神経障害性疼痛関連因子群の変化から解説する。さらに最近では、神経障害時に起こるLPA依存的な脱髄は脊髄近傍特異的な後根神経に生じることを明らかにしており、また他の痛みを伴う脱髄性疾患とLPAの関与についても紹介する。(著者抄録)
Hiroshi Ueda, Misaki Matsumoto
Folia Pharmacologica Japonica   131(5) 367-371   May 2008
脳を守るタンパク質プロサイモシンα 新しい脳卒中治療薬の開発にむけて
植田 弘師
Medical Bio   5(2) 83-89   Mar 2008
[Cancer pain model and morphine analgesia]
Ueda M, Ueda H
Nippon rinsho. Japanese journal of clinical medicine   65 2-4   Jan 2007   [Refereed]
【がん緩和医療 現状と展望】 がん性疼痛モデルとモルヒネの作用
植田 睦美, 植田 弘師
日本臨床   65(1) 2-4   Jan 2007
Hiroshi Ueda
Folia Pharmacologica Japonica   127(3) 161-165   Mar 2006
【慢性疼痛】 疼痛と受容体 リゾホスファチジン酸受容体
木口 倫一, 植田 弘師
治療学   39(8) 820-822   Aug 2005
Ueda H
Annals of the New York Academy of Sciences   1025 376-382   Oct 2004   [Refereed]
【痛みシグナルの制御機構と最新治療エビデンス】 疼痛の生理機構と分子メカニズム 神経因性疼痛誘発因子としてのリゾホスファチジン酸
植田 弘師, 井上 誠
医学のあゆみ   211(5) 411-414   Oct 2004
慢性疼痛疾患に共通する形態変化である脱髄に着目し,神経傷害時に産生されるリゾホスファチジン酸(LPA)が脱髄をはじめとする一連の神経因性疼痛病態を示すことを明らかにした.これらには疼痛過敏応答とアロディニアが含まれ,疼痛過敏に関連する遺伝子(Ca2+チャネル)や脊髄での増感作用に関与するPKCγの発現上昇が含まれる.一方で,神経傷害やLPA投与により誘発される,こうしたすべての分子機構は,その受容体LPA1遺伝子欠損動物において完全に消失した.以上,これらのことは,LPAが神経因性疼痛の誘...
Hiroshi Ueda
Biological and Pharmaceutical Bulletin   27 949   Jul 2004
Makoto Inoue, Md Harunor Rashid, Ryousuke Fujita, James J.A. Contos, Jerold Chun, Hiroshi Ueda
Nature Medicine   10 755   Jan 2004
Anti-opioid systems in morphine tolerance and addiction--locus-specific involvement of nociceptin and the NMDA receptor.
Ueda H
Novartis Foundation symposium   261 155-62; discussion 162   2004   [Refereed]
Ueda H
Nippon yakurigaku zasshi. Folia pharmacologica Japonica   122(3) 192-200   Sep 2003   [Refereed]
【病態としての"痛み"研究】 神経因性疼痛のメカニズム
井上 誠, 植田 弘師
脳21   6(1) 34-41   Jan 2003
神経因性疼痛は,神経系の一時的な損傷やその機能異常が原因となる,もしくはそれによって惹起される疼痛である.代表的な疼痛疾患としては,帯状疱疹後神経痛,三叉神経痛,幻肢痛,カウザルギーならびに糖尿病性神経因性疼痛などがある.特に,糖尿病患者は成人の10人に1人の割合で存在することから,糖尿病性神経因性疼痛は神経因性疼痛患者のうち上位に位置している.これら神経因性疼痛の発現機構を解明し,有効な治療法を確立するため,様々な実験動物モデルが開発されている.近年推測されている神経因性疼痛の発現機構を...
Ueda H, Hamabe W
Nippon yakurigaku zasshi. Folia pharmacologica Japonica   119(2) 79-88   Feb 2002   [Refereed]
H. Ueda, T. Matsumoto
Seikagaku   73 272-276   Dec 2001
H. Ueda, M. Inoue
Folia Pharmacologica Japonica   118(2) 89-95   Aug 2001
Neuropathic pain associated with abnormal tactile and thermal responses that are extraterritorial to the injured nerve is known to be difficult to diagnose and treat because of clinical observation of limited responsiveness to opioids and non-ster...
植田 弘師, 井上 誠
日本薬理学雑誌   118(2) 89-95   Aug 2001
神経因性疼痛は消炎鎮痛薬や麻薬性鎮痛薬に対し抵抗性を示す疼痛疾患である.その疾患としては帯状疱疹後神経痛,カウザルギー,三叉神経痛,糖尿病性神経炎などをはじめ数多く認められ,その苦痛は患者のQOLを著しく損なうものである.この発現機構を解明し有効な治療法を確立するために,これ迄に開発されてきた様々な実験動物モデルと評価に用いられる末梢性疼痛試験法について解説した
オピオイド受容体研究の新展開
植田 弘師, 松本 貴之
ペインクリニック   22(2) 195-202   Feb 2001
より安心してがん性疼痛治療を行うためには,麻薬性鎮痛薬の作用メカニズムやその可塑的調節機構などを理解することが重要である.μ,δ,κ,型オピオイド受容体の遺伝子クローニングに続くオピオイド受容体研究における新しい知見を次項により概説した.1)多種にわたる選択性スプライシング産物の存在,2)遺伝子欠損マウスにおけるオピオイド受容体の生理的意義,3)オピオイド関連ノシセプチン受容体のモルヒネ耐性形成における役割,4)オピオイド受容体発現細胞における受容体リン酸化と脱感作機構,5)受容体インター...
臨床に必要な神経化学 ニューレキシン
吉田 明, 植田 弘師
Clinical Neuroscience   19(2) 118-119   Feb 2001
【性ホルモンと精神神経機能】 ニューロステロイドに関する最近の知見 ニューロステロイドの生成過程と作用機序
吉田 明, 植田 弘師
脳の科学   22(1) 37-42   Jan 2000
Hiroshi Ueda, Makoto Inoue
Folia Pharmacologica Japonica   114(6) 347-356   Dec 1999
The family of the G protein-coupled opioid receptors was recently extended by a novel member that did not bind any of the typical opioid receptor ligands. Identification of the orphan receptor in this way led to the advent of 'reverse pharmacology...
H. Ueda, A. Yoshida
Folia Pharmacologica Japonica   114(1) 51-59   Jul 1999
Studies on the sigma receptor and related compounds are becoming more attractive since they were found to be closely related to higher brain functions such as memory, learning, depression, anxiety, schizophrenia and neuroprotection. Along with the...
オピオイド受容体 基礎から臨床への最前線
植田 弘師
LiSA   5(4) 324-344   Apr 1998
Yasuhisa Kuroda, Hiroshi Ueda, Hiroshi Nozawa, Hisanobu Ogoshi
Tetrahedron Letters   38 7901-7904   Nov 1997
The structures of six peptide mimics having different bulkiness and/or rigidity of the amino acids were investigated spectroscopically. Comparison of H NMR, IR spectra and H-D exchangerate of the amide protons reveals that 2-amino-2-carboxyadamant...
神経系の受容体とリン酸化
福嶋 伸之, 植田 弘師
最新医学   51(7) 1243-1251   Jul 1996
卵母細胞発現系における受容体 G蛋白再構成実験を利用した受容体同種脱感作機構の解析
植田 弘師, 林 千文
医学のあゆみ   175(4) 225-229   Oct 1995
神経系レセプターのリン酸化による機能調節と可塑性
佐々木 幸生, 植田 弘師
Clinical Neuroscience   13(5) 529-534   May 1995
Yoshimi Misu, Hiroshi Ueda, Yoshio Goshima
Advances in Pharmacology   32 427-459   Jan 1995
L-3,4-dihydroxyphenylalani (L-DOPA) is a precursor for transmitter dopamine as well as an endogenous potentiator of presynaptic P-adrenoceptors to facilitate the dopamine release and for postsynaptic D, receptors. L-DOPA may also be a neurotransmi...
Jin‐Liang ‐L Yue, Takeaki Miyamae, Hiroshi Ueda, Yoshimi Misu
Clinical and Experimental Pharmacology and Physiology   22    Jan 1995
1. Transmitter‐like L‐DOPA functions as a tonic to produce postsynaptic cardiopressor responses in the rostral ventrolateral medulla (RVLM) of rats. We attempted to clarify whether a transmitter‐like L‐DOPA system is altered in the RVLM of spontan...
Yoshimi Misu, Jin‐Liang ‐L Yue, Yoko Okumura, Takeaki Miyamae, Hiroshi Ueda
Clinical and Experimental Pharmacology and Physiology   22    Jan 1995
1. L‐DOPA as a probable neurotransmitter of baroreceptor afferents functions as a tonic to mediate cardiodepressor control in the nucleus tractus solitarii (NTS). We attempted to clarify further whether a transmitter‐like L‐DOPA system is altered ...
Yoshinori Tominaga, Koichiro Ogata, Hiroshi Ueda, Shinya Kohra, Akira Hosomi
Chemical and Pharmaceutical Bulletin   43 1425-1434   Jan 1995
N-Cyano- or N-(/Ntoluenesulfonyl)-N‘-(trimethyMlylmethyl)-S-methylisothiourea (3, 4), readily prepared by reactions of S, S'-dimethyl N-cyano- (la) and S, S'-dimethyl N-(p-toluenesulfonyl)- (lb) carbonimidodithioates with trimethylsilylmethylamine...
J. L. Yue, T. Miyamae, H. Ueda, Y. Misu
Japanese Heart Journal   36 519   Jan 1995
Hiroshi Ueda, Takeaki Miyamae, Nobuyuki Fukushima, Yoshimi Misu
Regulatory Peptides   54 305-306   Nov 1994
植田 弘師
日本薬理学雑誌   104(3) 229-239   Sep 1994
J. L. Yue, H. Ueda, Y. Goshima, Y. Misu
Japanese Heart Journal   35 538   Jan 1994
Hiroshi Ueda
Folia Pharmacologica Japonica   104 229-239   Jan 1994
Complementary DNAs encoding δ, μ and κ-opioid receptors have now been cloned and characterized. These receptors, which are members of the superfamily of seven transmembrane spanning receptors, share a high degree of amino acid sequence similarity ...
Shinya Kohra, Hiroshi Ueda, Yoshinori Tominaga
Heterocycles   36 2673-2676   Dec 1993
2-Trimethylsilylmethylthiothiazoline (1) reacted with aromatic aldehydes in the presence of cesium fluoride or tris(dimethylamino)sulfur(trimethylsilyl) difluoride (TASF) to give 2-heteroarylthioethanol (4) or thiiran (5) derivatives in good yield...
Shinya Kohra, Hiroshi Ueda, Yoshinori Tominaga
Heterocycles   36 1497-1500   Jul 1993
2-Trimethylsilylmethylthiopyridine prepared readily by the reaction of 2-mercaptopyridine with chloromethyltrimethylsilane in the presence of potassium carbonate reacts with carbonyl compounds in the presence of a catalytic amount of tetrabutylamm...
Yoshinori Tominaga, Hiroshi Ueda, Koichiro Ogata, Shinya Kohra, Makoto Hojo, Makoto Hojo, Masakazu Ohkuma, Masakazu Ohkuma, Kyoji Tomita, Kyoji Tomita, Akira Hosomi, Akira Hosomi
Tetrahedron Letters   33 85-88   Jan 1992
The title compounds, readily prepared by the reaction of the corresponding S-methyl N-(p-toluene- sulfonyl)dithioiminocarbonate and 2-mercaptothiazoline with (chloromethyl)trimethylsilane in the presence of a base, were used as new reagents for th...
M. Satoh, H. Ueda, S. Tamura, Y. Yoshihara, N. Fukushima
Advances in Experimental Medicine and Biology   287 97-110   Aug 1991
H. Ueda, J. Harada, K. Nishimura, K. Ishida, S. Uno, M. Satoh
Nippon rinsho. Japanese journal of clinical medicine   48 953-961   May 1990
M. Satoh, H. Ueda, H. Misawa, J. Harada, K. Nishimura, T. Katada, M. Ui
New leads in opioid research: proceedings of the International Narcotics Research Conference. ICS914   297-298   Jan 1990
The [3H][D-Pen2,D-Pen5]enkephalin ([3H]DPDPE) binding was markedly inhibited by GTPγS in both membrane preparations from striatum and ileal myenteric plexus of guinea-pig. DPDPE stimulated low-K(m) GTPase and inhibited adenylate cyclase in the lat...
オピオイドレセプター
佐藤 公道, 植田 弘師
Clinical Neuroscience   8(1) 28-29   Jan 1990
植田 弘師
日本薬理学雑誌   94(6) 339-349   Dec 1989
ジペプチド性神経活性物質キョートルフィンの生合成機構
植田 弘師, 吉原 良浩, 佐藤 公道
生化学   61(7) 592-596   Jul 1989
植田 弘師, 佐藤 公道
生物物理   29(2) 346-350   Apr 1989
H. Ueda
Folia Pharmacologica Japonica   94 339-349   Jan 1989
〔エンドルフィン〕実験動物におけるエンドルフィンの産生遊離
植田 弘師, 高木 博司, 猪木 令三
病態生理   6(4) 263-270   Apr 1987
T. Kubo, Y. Goshima, H. Ueda, Y. Misu
Journal of Hypertension   4    Jan 1986
エンケファリン遊離因子としてのキョートルフィン
高木博司, 植田弘師
蛋白質・核酸・酵素   26(2) 151-159   Feb 1981
H. Ueda, Y. Kuraishi, H. Shiomi, H. Takagi
Neuroscience Letters   23    Jan 1981
H. Shiomi, H. Ueda, H. Amano
Japanese Journal of Pharmacology   30    Jan 1980
H. Takagi, H. Shiomi, H. Ueda, H. Amano
Japanese Journal of Pharmacology   29    Jan 1979

Conference Activities & Talks

 
Centralized Painとしての線維筋痛症動物モデル 病態生理学と治療薬理学
植田弘師、根山広行、堂園直貴:
日本線維筋痛症学会第10回学術集会   29 Sep 2018   
脳虚血ストレスから脳を守るDAMPs/Alarminsプロサイモシンα
植田弘師、岩元隆征:
第40回日本生物学的精神医学会・第61回日本神経化学会大会合同年会   8 Sep 2018   
Prothymosin α plays multifunctional robustness roles against fatal stresses in neurons. [Invited]
Ueda H:
京都大学iPS細胞研究所   7 Aug 2018   
脳虚血時の神経保護機能を有するDAMPsプロサイモシンα
植田弘師:
第41回日本神経科学大会   29 Jul 2018   
【Invited Lectures】Lysophosphatidic acid signaling is involved in the development and maintenance of neuropathic pain and fibromyalgia. [Invited]
Ueda H:
the 18th World Congress of Basic and Clinical Pharmacology(WCP2018)   2 Jul 2018   
tPA誘発性脳卒中後疼痛CPSPマウスモデルとLPAの関与
植田弘師:
第40回日本疼痛学会   15 Jun 2018   
「Centralized Pain」について [Invited]
植田弘師:
第40回日本疼痛学会   15 Jun 2018   
脳卒中後疼痛研究の最前線 tPA誘発性脳卒中後疼痛CPSPマウスモデルとLPAの関与 [Invited]
植田 弘師
第40回日本疼痛学会   15 Jun 2018   
植田弘師
日本慢性疼痛学会プログラム・抄録集   16 Feb 2018   
脳を守るDAMPs分子プロサイモシンαの分子神経生物学と創薬研究
植田弘師:
信州大学バイオメディカル研究所特別セミナー   4 Dec 2017   
Recent Advances in Neurobiology of Prothymosin α1 Non-Classical Release and New Receptor System.
Ueda H:
5th International Symposium on Thymosins in Health and Disease   16 Nov 2017   
断続的繰り返し精神ストレス(Empathy)による新しい線維筋痛症モデルとLPAシグナルを介するメカニズム
植田弘師:
日本線維筋痛症学会第9回学術集会   14 Oct 2017   
慢性疼痛時のモルヒネ感受性低下のメカニズムにもとづく治療と創薬
植田弘師:
第37回鎮痛薬・オピオイドペプチドシンポジウム   9 Sep 2017   
Brain mechanisms of LPA-signaling in the central pain.
Ueda H,Neyama H:
2017 FASEB (Federation of American Societies for Experimental Biology )   24 Aug 2017   
Therapeutic recovery from diminished morphine analgesia in chronic pain state.
Ueda H,Neyama H:
The International Narcotics Research Conference 2017   11 Jul 2017   
痛みメモリーを消去するLPA シグナル制御創薬研究、
植田弘師:
平成29年度 東北医科薬科大学  創薬研究センターシンポジウム   17 Jun 2017   
プロサイモシンα: ストレスから脳を守るDAMPs/Alarmins分子、
植田弘師:
第90回日本薬理学会   15 Mar 2017   
Fibromyalgia in mice.
Ueda H:
GLORIA symposium (glial-opioid-receptor-interface in analgesia symposium)   2 Dec 2016   
Brain Mechanisms and Pharmacotherapy in Generalized Chronic Pain Model Similar to Fibromyalgia in Mice.
Ueda H:
Fibromyalgia Research Symposium 2016 in Nagasaki (FRS 2016NAGASAKI)   1 Oct 2016   
Neuropathic pain initiation and maintenance: the role of glialーmediated LPA signaling in neuropathic pain models .
Ueda H:
16th World Congress on Pain (IASP)   28 Sep 2016   
Lysophosphatidic acid: a biochemical signature for neuropathic pain.
Ueda H:
16th World Congress on Pain (IASP)   28 Sep 2016   
Pharmacotherapeutic innovation using a novel experimental fibromyalgia model in mice.
Ueda H:
Pain Mechanisms and Therapeutics Conference   10 Jun 2016   
慢性疼痛標的としてのリゾホスファチジン酸受容体の構造と機能
植田弘師
第13回GPCR研究会   13 May 2016   
慢性疼痛のアカデミア創薬シーズとしてのリゾホスファチジン酸
植田弘師
久光製薬 『第8回痛みを考える会』   19 Mar 2016   
AMED長崎大学アカデミア創薬拠点におけるGPCR関連創薬研究
植田弘師
MOE 2015 リリースセミナー   10 Dec 2015   
モルヒネ感受性の低下する慢性の痛みのしくみについて
植田弘師
第19回島根癌疼痛緩和研究会   31 Oct 2015   
マウス断続的冷温ストレスならびにくり返し筋肉損傷ストレスにより誘発される 全身性疼痛モデルにおける薬理学的特性の比較
植田弘師、迎武紘、根山広行、遠藤洋二郎、河本綜一郎
日本線維筋痛症学会 第7回学術集会   2 Oct 2015   
慢性疼痛の陰性症状とエピジェネティクス
植田弘師
第58回日本神経化学会大会   11 Sep 2015   
「LPA as chemical signature of neuropathic pain ? mechanisms and therapeutic innovation」.
Ueda H:
FASEB Science Research Conference   26 Aug 2015   
文科省創薬PF事業における長崎大学アカデミア創薬拠点活動 〜感染症、放射線障害創薬における低分子医薬の探索〜
植田弘師
GE Life Sciences Day 2015   24 Jul 2015   
Pharmacotherapeutic innovation against LPA-mediated chronic pain.
Ueda H:
14th International Conference (the Bioactive Lipid Mediators in Cancer Inflammation and Related Diseases)   15 Jul 2015   
神経障害性疼痛のメカニズムにおけるフィードフォワード機構
植田弘師
第36回 日本疼痛学会   3 Jul 2015   
リゾホスファチジン酸を介する慢性疼痛の形成と維持機構について
植田弘師
『第11回 関西地区化合物スクリーニング講習会』   11 Mar 2015   
Differential regulation of endocannabinoids and LPA production in inflammatory and neuropathic pain.
Ueda H, Nagai J Mukae T:
6th international conference on Phospholipase A2 and Lipid Mediators(PLM2015)   10 Feb 2015   
Prothymosin alpha-derived Hexapeptide and its analogs ameliorate blood-brain barrier dysfunction following cerebral ischemia in mice“.
Ueda H:
FOURTH INTERNATIONAL SYMPOSIUM ON THYMOSINS IN HEALTH AND DISEASE   2014   
Epigenetic mechanisms for pain: A novel approach to pain treatment.
Ueda H:
IASP 15th World Congress on Pain   2014   
My Phenotypic Switch Studies.
Ueda H:
Caltech Neuroimmunology Symposium   2014   
リゾホスフアチジン酸生合成の自己増幅と慢性疼痛機構
植田弘師
長崎大学医学部シンポジウム 「脳神経系の分子病態・治療研究の最前線」   2014   
線維筋痛症の動物モデルの特徴と治療薬理学的考察
植田弘師
アステラス製薬 筑波研究センター講演会   2014   
線維筋痛症の動物モデルと薬物治療
植田弘師
第10回日本疲労学会総会学術集会   2014   
疼痛に関する最新の知見
植田弘師
キッセイ薬品工業株式会社中央研究所セミナー   2014   
ストレスにより誘発される慢性痛のしくみと創薬薬理
植田弘師
日本ストレス学会学術集会第30回記念大会   2014   
Blockade of lysophosphatidic acid receptor signaling completely cures the established chronic pain.
Ueda H, Nagai J, Mukae T, Matsushita Y
13th Int1l Conference on Bioactive Lipids in Cancer, Inflammation and Related Diseases   2013   
Lysophosphatidic acid: Chemical signature of neuropathic pain.
Ueda H:
The 92nd Annual Meeting of the German Physiological Society   2013   
神経障害性疼痛における脂質メデイエーターの役割
植田弘師
Cinderella研究会   2013   
慢性疼痛とリゾホスファチジン酸(LPA)
植田弘師
第46回広島神経医科学研究会   2013   
Central pain and lysophosphatidic acid
Ueda H, Nagai J, Mukae T
FASEB SCIENCE RESEARCH CONFERENCE- Lysophospholipid and Other Related Mediators - From Bench to Clinic   2013   
「蛍光と創薬」神経保護蛋白質プロサイモシンαの発見から脳梗塞治療創薬へ
植田弘師
第1回最先端創薬科学シンポジウム   2013   
Repeated challenges of systemic mirtazapine cause permanent pain relief in mouse experimental fibromyalgia model.
Ueda H:
IASP 14th World Congress on Pain   2012   
Epigenetic silencing of sodium channel, TRP channels and opioid receptor in neuropathic pain.
Ueda H:
IASP 14th World Congress on Pain   2012   
Prothymosin alpha: its mechanisms for non-vesucular release and receptor in central nervous system.
Ueda H:
THIRD INTERNATIONAL SYMPOSIUM ON THYMOSINS IN HEALTH AND DISEASE   2012   
多様な慢性疼痛の初発・維持に関与する鍵分子リゾホスファチジン酸、
植田弘師
宮崎痛みの研究会講演、   2012   
長崎大学アカデミア創薬拠点事業、
植田弘師
第132回日本薬学会、   2012   
慢性痛動物モデルにおけるLPAを介する痛みのメカニズムと痛み治療のしくみ
植田弘師
日本ペインクリニック学会第46回大会   2012   
様々な慢性疼痛モデルの開発と治療薬開発のための病態分子生理学機構解析
植田弘師
新日本科学セミナー   2012   
長崎大学創薬拠点 『化合物ライブラリーを活用した放射糠障害防護剤スクリーニング』
植田弘師、鈴木啓司
日本放射線影響学会第55回大会   2012   
慢性疼痛のしくみ:神経障害性疼痛から線維筋痛症まで
植田弘師
日本線維筋痛症学会 第4回学術集会   2012   
線維筋痛症動物モデルにおける薬物治療
植田弘師
日本線維筋痛症学会 第4回学術集会   2012   
慢性疼痛とバイオマーカーに関する最近の研究
植田弘師
日本線維筋痛症学会 第4回学術集会   2012   
長崎大学創薬拠点の紹介とFDSSを用いたスクリーニング研究
植田弘師
FDSSセミナー   2012   
Molecular mechanism of chronic neuropathic pain.
Ueda H:
Bio-Rheumatology International Congress(BRIC) TOKYO The 8th GRAN Meeting   2011   
Prothymosin α: a novel neuroprotetive polypeptide against ischemic damages.
Ueda H:
2011 Taiwan-Japan Joint Symposium on Cell Signaling and Gene Regulation   2011   
LPA receptor-mediated amplification of LPA biosynthesis and demyelination underlie the initiation mechanisms for neuropathic pain.
Ueda H, Nagai J, Lin Ma, Yano R, Shinohara K, Shinagawa A, and Taira K:
The 9th IASP Research Symposium   2011   
Feed-forward amplification of LPA3 receptor-mediated LPA production via microglia in the initiation of neuropathic pain.
Ueda H, Nagai J, Ma L, and Taira K:
FASEB SUMMER RESEARCH CONFERENCE- Lysophospholipid Mediators in Health & Disease-   2011   
Lysophosphatidic acid as initiator of neuropathic pain - biosynthesis and demyelination.
UEDA H:
The 4th Asian Pain Symposium   2011   
虚血性疾患に対する新規神経保護性ポリペプチド:プロサイモシンα、
植田 弘師、松永 隼人
第84回日本薬理学会年会、   2011   
慢性疼痛機構におけるフィードフォワード性LPA生合成増幅機構、
植田弘師
日本分子生物学会 第11回春季シンポジウム、   2011   
線維筋痛症動物モデルにおける薬物治療、
植田弘師
日本線維筋痛症学会 第3回学術集会、   2011   
"Rescue of specific promotor-regulated mu-opioid and nmda receptor gene into pag of k/o mice - pain species-specific brain loci for morphine analgesia and tolerance".
UEDA H:
IASP The 13th World Congress on Pain,   2010   
Epigenetic control of opioid receptor gene expression in neuropathic pain model.
UEDA H:
INRC 2010,   2010   
慢性疼痛時の神経可塑性を担うリゾホスファチジン酸、
植田弘師
第39回日本慢性疼痛学会、   2010   
慢性疼痛の初発原因分子としてのリゾホスファチジン酸 ?フィードフォワード性 de novo LPA合成、
植田弘師
第52回脂質生化学会、   2010   
神経障害性疼痛における de novo リゾホスファチジン酸の生合成を介するフィードフォワード機構、
植田弘師
第32回日本疼痛学会、   2010   
Feed-forward system of peripheral and central chronic pain through lysophosphatidic acid (リゾホスファチジン酸を介した末梢性および中枢性の慢性痛のフィードフォワード性増幅機構)、
植田弘師
第53回日本神経化学会、   2010   
病態時のオピオイド鎮痛、
植田弘師
第6回痛みの治療研究会、   2010   
脳虚血及び網膜虚血を保護するプロサイモシンα、
植田弘師
第2回Neuroprotective Meeting for Young Researcher、   2010   
モルヒネによる痒み誘発と末梢性鎮痛効果に関する最近の話題、
植田弘師
第20回国際痒みシンポジウム、   2010   
線維筋痛症の痛みの分子生理・薬理学、
植田弘師
日本線維筋痛症学会 第2回学術集会、   2010   
末梢神経性の神経障害性疼痛発生機序、
植田弘師
平成22年度岡崎生理研研究会、   2010   
"Identification of prothymosin alpha, the necrosis-apoptosis switch molecule in ischemic culture of cortical neuron".
UEDA H:
Second International Symposium on Thymosins in Health and Disease,   2009   
Neural pathological roles for receptor mediated LPA signaling.
UEDA H:
FASEB SUMMER RESEARCH CONFERENCE “Lysophospholipid Mediators in Health and Disease”   2009   
エピジェノミクス制御物質クルクミンによるモルヒネ耐性抑制とBDNF産生制御
Ueda H
第129年会日本薬学会   2009   
神経の可塑性について─慢性疼痛機構におけるフィードフォワード増幅機構─
植田弘師
第23回日本ニューロモデュレーション学会   2009   
神経因性疼痛とリゾホスファチジン酸生合成
植田弘師
第7回整形外科痛みを語る会   2009   
慢性痛における神経可塑性を担うエピジェネティクス異常
植田弘師
第32回日本神経科学大会   2009   
Feed-forward mechanisms of chronic pain through de novo LPA synthesis
Ueda H
第4回九大痛みの研究会   2009   
神経障害性疼痛の機序と今後の研究の展望
植田弘師
平成21年度厚生労働科学研究費補助金「鍼灸を含めた内因性鎮痛法の機序の解明およびがん緩和医療における臨床的適応に関する研究」   2009   
「痛みとオピオイド研究の最新の話題ーモルヒネに抵抗性の痛みのメカニズムー」
植田弘師
第37回和歌山悪性腫瘍研究会   2009   
Experimental Models for Thalamic Pain and Fibromyalgia.
UEDA H:
APLAR2008(13TH CONGRESS OF THE ASIA PACIFIC LEAGUE OF ASSOCIATIONS FOR RHEUMATOLOGY).   2008   
Intermittent cold stress causes a long-term allodynia and hyperalgesia in mice, a model for generalized chronic pain syndrome or fibromyalgia
UEDA H:
国際疲労学会(International Conference on Fatigue Science 2008).   2008   
Sustained central sensitization of pain following lysophosphatidic acid injection into thalamus
UEDA H:
AsianPain2008 第3回 アジアンペインシンポジウム、第30回 日本疼痛学会   2008   
脳卒中の神経細胞死を抑えるタンパク質プロサイモシン アルファの発見
植田弘師
日本ポリアミン研究会第22回研究発表会   2008   
慢性疼痛の分子機構
植田弘師
「痛み克服の国際的研究教育拠点の形成」キックオフシンポジウム   2008   
細胞死モードスイッチ機構を介した新規神経保護分子プロサイモシンアルファーの発見
植田弘師
第81回日本薬理学会   2008   
ネクローシス性神経細胞死抑制作用を有する新規蛋白質プロサイモシン・アルファの発見
植田弘師
日本薬学会第128年会   2008   
リゾホスファチジン酸受容体と神経因性疼痛
植田弘師
第5回GPCR研究会   2008   
Prothymosin-alpha as a novel anti-ischemic neuroprotective protein
Ueda H
Neuroscience2008 第31回日本神経科学大会   2008   
化学療法に伴う神経因性疼痛のメカニズム
植田弘師
第41回日本整形外科学会 骨・軟部腫瘍学術集会   2008   
脳梗塞時の脳保護に働くネクローシス抑制タンパク質、プロサイモシンアルファの発見とその機能解明
植田弘師
第6回鹿児島ニューロフォーラム   2008   
Prothymosin αによるアポトーシス誘導を介した神経ネクローシス抑制
植田弘師
BMB2008 (第31回日本分子生物学会年会・第81回日本生化学会大会 合同大会).   2008   

Education

 
Apr 1978
 - 
Mar 1981
Kyoto University
 
Apr 1976
 - 
Mar 1978
Kyoto University
 
Apr 1972
 - 
Mar 1976
Department of Pharmacy, Kyoto University