17 results on '"Otani, Yoshinori"'
Search Results
2. Influence of novel readthrough agents on myelin protein zero translation in the peripheral nervous system
- Author
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Otani, Yoshinori, Taguchi, Akihiro, Hamada, Keisuke, Hayashi, Yoshio, Yamaguchi, Yoshihide, and Baba, Hiroko
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- 2022
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3. Deformation behavior and acting earth pressure of three-hinge precast arch culvert in construction process
- Author
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Sawamura, Yasuo, Ishihara, Hiroyuki, Otani, Yoshinori, Kishida, Kiyoshi, and Kimura, Makoto
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- 2019
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4. Upregulation of large myelin protein zero leads to Charcot–Marie–Tooth disease-like neuropathy in mice
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Otani, Yoshinori, Ohno, Nobuhiko, Cui, Jingjing, Yamaguchi, Yoshihide, and Baba, Hiroko
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- 2020
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5. MELAS-Derived Neurons Functionally Improve by Mitochondrial Transfer from Highly Purified Mesenchymal Stem Cells (REC).
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Liu, Lu, Yang, Jiahao, Otani, Yoshinori, Shiga, Takahiro, Yamaguchi, Akihiro, Oda, Yasuaki, Hattori, Miho, Goto, Tsukimi, Ishibashi, Shuichi, Kawashima-Sonoyama, Yuki, Ishihara, Takaya, Matsuzaki, Yumi, Akamatsu, Wado, Fujitani, Masashi, and Taketani, Takeshi
- Subjects
MESENCHYMAL stem cells ,INDUCED pluripotent stem cells ,MITOCHONDRIAL DNA ,MITOCHONDRIA ,NEURONS ,PLANT mitochondria ,INTRACELLULAR calcium - Abstract
Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome, caused by a single base substitution in mitochondrial DNA (m.3243A>G), is one of the most common maternally inherited mitochondrial diseases accompanied by neuronal damage due to defects in the oxidative phosphorylation system. There is no established treatment. Our previous study reported a superior restoration of mitochondrial function and bioenergetics in mitochondria-deficient cells using highly purified mesenchymal stem cells (RECs). However, whether such exogenous mitochondrial donation occurs in mitochondrial disease models and whether it plays a role in the recovery of pathological neuronal functions is unknown. Here, utilizing induced pluripotent stem cells (iPSC), we differentiated neurons with impaired mitochondrial function from patients with MELAS. MELAS neurons and RECs/mesenchymal stem cells (MSCs) were cultured under contact or non-contact conditions. Both RECs and MSCs can donate mitochondria to MELAS neurons, but RECs are more excellent than MSCs for mitochondrial transfer in both systems. In addition, REC-mediated mitochondrial transfer significantly restored mitochondrial function, including mitochondrial membrane potential, ATP/ROS production, intracellular calcium storage, and oxygen consumption rate. Moreover, mitochondrial function was maintained for at least three weeks. Thus, REC-donated exogenous mitochondria might offer a potential therapeutic strategy for treating neurological dysfunction in MELAS. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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6. Influence of transient flooding on steel strip reinforced soil walls
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Miyata, Yoshihisa, Bathurst, Richard J., Otani, Yoshinori, Ohta, Hitoshi, and Miyatake, Hiroaki
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- 2015
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7. Mechanism of Bearing Capacity of Spread Footings Reinforced with Micropiles
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Tsukada, Yukihiro, Miura, Kinya, Tsubokawa, Yukitomo, Otani, Yoshinori, and You, Guan-Lin
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- 2006
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8. Maternal and Adult Interleukin-17A Exposure and Autism Spectrum Disorder.
- Author
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Fujitani, Masashi, Miyajima, Hisao, Otani, Yoshinori, and Liu, Xinlang
- Subjects
AUTISM spectrum disorders ,MATERNAL immune activation ,AUTOIMMUNE diseases ,INTERLEUKIN-17 ,ADULTS - Abstract
Epidemiological evidence in humans has suggested that maternal infections and maternal autoimmune diseases are involved in the pathogenesis of autism spectrum disorder. Animal studies supporting human results have shown that maternal immune activation causes brain and behavioral alterations in offspring. Several underlying mechanisms, including interleukin-17A imbalance, have been identified. Apart from the pro-inflammatory effects of interleukin-17A, there is also evidence to support the idea that it activates neuronal function and defines cognitive behavior. In this review, we examined the signaling pathways in both immunological and neurological contexts that may contribute to the improvement of autism spectrum disorder symptoms associated with maternal blocking of interleukin-17A and adult exposure to interleukin-17A. We first describe the epidemiology of maternal immune activation then focus on molecular signaling of the interleukin-17 family regarding its physiological and pathological roles in the embryonic and adult brain. In the future, it may be possible to use interleukin-17 antibodies to prevent autism spectrum disorder. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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- View/download PDF
9. CHRONIC PERIPHERAL NERVE COMPRESSION DISRUPTS PARANODAL AXOGLIAL JUNCTIONS
- Author
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Otani, Yoshinori, Yermakov, Leonid M., Dupree, Jeffrey L., and Susuki, Keiichiro
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Ankyrins ,Arthrogryposis ,Cell Adhesion Molecules, Neuronal ,Neural Conduction ,Evoked Potentials, Motor ,Sciatic Nerve ,Article ,Functional Laterality ,Mice, Inbred C57BL ,Disease Models, Animal ,Mice ,Shab Potassium Channels ,Gene Expression Regulation ,Microscopy, Electron, Transmission ,Ranvier's Nodes ,Animals ,Female ,Nerve Growth Factors ,Hereditary Sensory and Motor Neuropathy ,Cell Adhesion Molecules - Abstract
Peripheral nerves are often exposed to mechanical stress leading to compression neuropathies. The pathophysiology underlying nerve dysfunction by chronic compression is largely unknown.We analyzed molecular organization and fine structures at and near nodes of Ranvier in a compression neuropathy model in which a silastic tube was placed around the mouse sciatic nerve.Immunofluorescence study showed that clusters of cell adhesion complex forming paranodal axoglial junctions were dispersed and overlapped frequently with juxtaparanodal components. These paranodal changes occurred without internodal myelin damage. The distribution and pattern of paranodal disruption suggests that these changes are the direct result of mechanical stress. Electron microscopy confirmed loss of paranodal axoglial junctions.Our data show that chronic nerve compression disrupts paranodal junctions and axonal domains required for proper peripheral nerve function. These results provide important clues toward better understanding of the pathophysiology underlying nerve dysfunction in compression neuropathies. Muscle Nerve 55: 544-554, 2017.
- Published
- 2016
10. Chronic peripheral nerve compression disrupts paranodal axoglial junctions.
- Author
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Otani, Yoshinori, Yermakov, Leonid M., Dupree, Jeffrey L., and Susuki, Keiichiro
- Subjects
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ANIMAL experimentation , *ANIMALS , *ARTHROGRYPOSIS , *BIOLOGICAL models , *CELL adhesion molecules , *CELL membranes , *CEREBRAL dominance , *CHARCOT-Marie-Tooth disease , *ELECTRON microscopy , *EVOKED potentials (Electrophysiology) , *GENES , *GLYCOPROTEINS , *MICE , *NERVE growth factor , *NEURAL conduction , *RESEARCH funding , *SCIATIC nerve - Abstract
Introduction: Peripheral nerves are often exposed to mechanical stress leading to compression neuropathies. The pathophysiology underlying nerve dysfunction by chronic compression is largely unknown.Methods: We analyzed molecular organization and fine structures at and near nodes of Ranvier in a compression neuropathy model in which a silastic tube was placed around the mouse sciatic nerve.Results: Immunofluorescence study showed that clusters of cell adhesion complex forming paranodal axoglial junctions were dispersed and overlapped frequently with juxtaparanodal components. These paranodal changes occurred without internodal myelin damage. The distribution and pattern of paranodal disruption suggests that these changes are the direct result of mechanical stress. Electron microscopy confirmed loss of paranodal axoglial junctions.Conclusions: Our data show that chronic nerve compression disrupts paranodal junctions and axonal domains required for proper peripheral nerve function. These results provide important clues toward better understanding of the pathophysiology underlying nerve dysfunction in compression neuropathies. Muscle Nerve 55: 544-554, 2017. [ABSTRACT FROM AUTHOR]- Published
- 2017
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11. Submembranous cytoskeletons stabilize nodes of Ranvier.
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Susuki, Keiichiro, Otani, Yoshinori, and Rasband, Matthew N.
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CYTOSKELETAL proteins , *NODES of Ranvier , *ACTION potentials , *SODIUM channels , *CELL adhesion , *PROTEOLYSIS , *MENTAL illness - Abstract
Rapid action potential propagation along myelinated axons requires voltage-gated Na + (Nav) channel clustering at nodes of Ranvier. At paranodes flanking nodes, myelinating glial cells interact with axons to form junctions. The regions next to the paranodes called juxtaparanodes are characterized by high concentrations of voltage-gated K + channels. Paranodal axoglial junctions function as barriers to restrict the position of these ion channels. These specialized domains along the myelinated nerve fiber are formed by multiple molecular mechanisms including interactions between extracellular matrix, cell adhesion molecules, and cytoskeletal scaffolds. This review highlights recent findings into the roles of submembranous cytoskeletal proteins in the stabilization of molecular complexes at and near nodes. Axonal ankyrin–spectrin complexes stabilize Nav channels at nodes. Axonal protein 4.1B–spectrin complexes contribute to paranode and juxtaparanode organization. Glial ankyrins enriched at paranodes facilitate node formation. Finally, disruption of spectrins or ankyrins by genetic mutations or proteolysis is involved in the pathophysiology of various neurological or psychiatric disorders. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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12. Stability of steel reinforced soil walls after footing failure.
- Author
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Bathurst, Richard J., Miyata, Yoshihisa, Otani, Yoshinori, Ohta, Hitoshi, and Miyatake, Hiroaki
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STEEL strip ,REINFORCED soils ,SOIL classification ,CONCRETE footing design & construction ,CIVIL engineering - Abstract
Two nominal identical 4 m high steel strip reinforced soil walls varying only with respect to reinforcement layer length arrangement were constructed and instrumented in an indoor laboratory environment. A novel feature of the tests was a foundation arrangement that allowed for simulated loss of toe support. Both walls performed well at the end of construction (EOC). Predicted unfactored maximum reinforcement tensile loads at the EOC using four different load models were judged to be conservative (safe for design) based on comparison with measured loads for both walls. Reinforcement loads were observed to increase with decreasing toe support, particularly at the base of the walls. A fully developed composite soil failure mechanism propagating from the heel of the foundation bulkhead and behind the reinforcement layers was observed during excavation of the stepped base wall model. There were no visual indications of soil failure within or behind the wall with longer uniform reinforcement lengths. However, predicted EOC loads for this wall were exceeded for most layers after loss of toe support. Implications for the design, analysis and performance of steel strip reinforced soil walls with similar reinforcement arrangements constructed over initially competent soil foundations and then subject to loss of toe support are identified. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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13. PLD4 Is Involved in Phagocytosis of Microglia: Expression and Localization Changes of PLD4 Are Correlated with Activation State of Microglia.
- Author
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Otani, Yoshinori, Yamaguchi, Yoshihide, Sato, Yumi, Furuichi, Teiichi, Ikenaka, Kazuhiro, Kitani, Hiroshi, and Baba, Hiroko
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MICROGLIA , *PHAGOCYTOSIS , *PHOSPHOLIPASE D , *CELLS , *LABORATORY mice - Abstract
Phospholipase D4 (PLD4) is a recently identified protein that is mainly expressed in the ionized calcium binding adapter molecule 1 (Iba1)-positive microglia in the early postnatal mouse cerebellar white matter. Unlike PLD1 and PLD2, PLD4 exhibits no enzymatic activity for conversion of phosphatidylcholine into choline and phosphatidic acid, and its function is completely unknown. In the present study, we examined the distribution of PLD4 in mouse cerebellar white matter during development and under pathological conditions. Immunohistochemical analysis revealed that PLD4 expression was associated with microglial activation under such two different circumstances. A primary cultured microglia and microglial cell line (MG6) showed that PLD4 was mainly present in the nucleus, except the nucleolus, and expression of PLD4 was upregulated by lipopolysaccharide (LPS) stimulation. In the analysis of phagocytosis of LPS-stimulated microglia, PLD4 was co-localized with phagosomes that contained BioParticles. Inhibition of PLD4 expression using PLD4 specific small interfering RNA (siRNA) in MG6 cells significantly reduced the ratio of phagocytotic cell numbers. These results suggest that the increased PLD4 in the activation process is involved in phagocytosis of activated microglia in the developmental stages and pathological conditions of white matter. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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14. Phospholipase D Family Member 4, a Transmembrane Glycoprotein with No Phospholipase D Activity, Expression in Spleen and Early Postnatal Microglia.
- Author
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Yoshikawa, Fumio, Banno, Yoshiko, Otani, Yoshinori, Yamaguchi, Yoshihide, Nagakura-Takagi, Yuko, Morita, Noriyuki, Sato, Yumi, Saruta, Chihiro, Nishibe, Hirozumi, Sadakata, Tetsushi, Shinoda, Yo, Hayashi, Kanehiro, Mishima, Yuriko, Baba, Hiroko, and Furuichi, Teiichi
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MICROGLIA ,PHOSPHOLIPASES ,LECITHIN ,GLYCOPROTEIN synthesis ,MEMBRANE distillation ,IN situ hybridization ,IMMUNOHISTOCHEMISTRY ,IMMUNOCYTOCHEMISTRY ,CORPUS callosum - Abstract
Background: Phospholipase D (PLD) catalyzes conversion of phosphatidylcholine into choline and phosphatidic acid, leading to a variety of intracellular signal transduction events. Two classical PLDs, PLD1 and PLD2, contain phosphatidylinositide-binding PX and PH domains and two conserved His-x-Lys-(x)
4 -Asp (HKD) motifs, which are critical for PLD activity. PLD4 officially belongs to the PLD family, because it possesses two HKD motifs. However, it lacks PX and PH domains and has a putative transmembrane domain instead. Nevertheless, little is known regarding expression, structure, and function of PLD4. Methodology/Principal Findings: PLD4 was analyzed in terms of expression, structure, and function. Expression was analyzed in developing mouse brains and non-neuronal tissues using microarray, in situ hybridization, immunohistochemistry, and immunocytochemistry. Structure was evaluated using bioinformatics analysis of protein domains, biochemical analyses of transmembrane property, and enzymatic deglycosylation. PLD activity was examined by choline release and transphosphatidylation assays. Results demonstrated low to modest, but characteristic, PLD4 mRNA expression in a subset of cells preferentially localized around white matter regions, including the corpus callosum and cerebellar white matter, during the first postnatal week. These PLD4 mRNA-expressing cells were identified as Iba1-positive microglia. In nonneuronal tissues, PLD4 mRNA expression was widespread, but predominantly distributed in the spleen. Intense PLD4 expression was detected around the marginal zone of the splenic red pulp, and splenic PLD4 protein recovered from subcellular membrane fractions was highly N-glycosylated. PLD4 was heterologously expressed in cell lines and localized in the endoplasmic reticulum and Golgi apparatus. Moreover, heterologously expressed PLD4 proteins did not exhibit PLD enzymatic activity. Conclusions/Significance: Results showed that PLD4 is a non-PLD, HKD motif-carrying, transmembrane glycoprotein localized in the endoplasmic reticulum and Golgi apparatus. The spatiotemporally restricted expression patterns suggested that PLD4 might play a role in common function(s) among microglia during early postnatal brain development and splenic marginal zone cells. [ABSTRACT FROM AUTHOR]- Published
- 2010
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15. Do Neurotrophins Connect Neurological Disorders and Heart Diseases?
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Fujitani, Masashi, Otani, Yoshinori, and Miyajima, Hisao
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NEUROLOGICAL disorders , *NEUROTROPHINS , *HEART diseases , *HYPOTHALAMUS , *NERVE growth factor , *BRAIN-derived neurotrophic factor , *CARDIOVASCULAR system - Abstract
Neurotrophins (NTs) are one of the most characterized neurotrophic factor family members and consist of four members in mammals. Growing evidence suggests that there is a complex inter- and bi-directional relationship between central nervous system (CNS) disorders and cardiac dysfunction, so-called "brain–heart axis". Recent studies suggest that CNS disorders, including neurodegenerative diseases, stroke, and depression, affect cardiovascular function via various mechanisms, such as hypothalamic–pituitary–adrenal axis augmentation. Although this brain–heart axis has been well studied in humans and mice, the involvement of NT signaling in the axis has not been fully investigated. In the first half of this review, we emphasize the importance of NTs not only in the nervous system, but also in the cardiovascular system from the embryonic stage to the adult state. In the second half, we discuss the involvement of NTs in the pathogenesis of cardiovascular diseases, and then examine whether an alteration in NTs could serve as the mediator between neurological disorders and heart dysfunction. The further investigation we propose herein could contribute to finding direct evidence for the involvement of NTs in the axis and new treatment for cardiovascular diseases. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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16. Pathophysiological Roles of Abnormal Axon Initial Segments in Neurodevelopmental Disorders.
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Fujitani, Masashi, Otani, Yoshinori, and Miyajima, Hisao
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NEURAL development , *AXONS , *ION channels , *NEURAL circuitry , *REGULATOR genes , *SYNAPSES , *BIOMARKERS - Abstract
The 20–60 μm axon initial segment (AIS) is proximally located at the interface between the axon and cell body. AIS has characteristic molecular and structural properties regulated by the crucial protein, ankyrin-G. The AIS contains a high density of Na+ channels relative to the cell body, which allows low thresholds for the initiation of action potential (AP). Molecular and physiological studies have shown that the AIS is also a key domain for the control of neuronal excitability by homeostatic mechanisms. The AIS has high plasticity in normal developmental processes and pathological activities, such as injury, neurodegeneration, and neurodevelopmental disorders (NDDs). In the first half of this review, we provide an overview of the molecular, structural, and ion-channel characteristics of AIS, AIS regulation through axo-axonic synapses, and axo−glial interactions. In the second half, to understand the relationship between NDDs and AIS, we discuss the activity-dependent plasticity of AIS, the human mutation of AIS regulatory genes, and the pathophysiological role of an abnormal AIS in NDD model animals and patients. We propose that the AIS may provide a potentially valuable structural biomarker in response to abnormal network activity in vivo as well as a new treatment concept at the neural circuit level. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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17. Microglial phospholipase D4 deficiency influences myelination during brain development.
- Author
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Chiba T, Otani Y, Yamaguchi Y, Ishibashi T, Hayashi A, Tanaka KF, Yamazaki M, Sakimura K, and Baba H
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- Animals, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Astrocytes metabolism, Cerebellum cytology, Corpus Callosum metabolism, Exonucleases, Membrane Glycoproteins metabolism, Mice, Neurons metabolism, Purkinje Cells metabolism, Brain embryology, Membrane Glycoproteins deficiency, Microglia enzymology, Myelin Sheath metabolism
- Abstract
Phospholipase D4 (PLD4) is expressed in activated microglia that transiently appear in white matter during postnatal brain development. Previous knockdown experiments using cultured microglia showed PLD4 involvement in phagocytosis and proliferation. To elucidate the role of PLD4 in vivo, PLD4-deficient mice were generated and the cerebella were examined at postnatal day 5 (P5) and P7, when PLD4 expression is highest in microglia. Wild type microglia showed strong immunoreactivity for microglial marker CD68 at P5, whereas CD68 signals were weak in PLD4-deficient microglia, suggesting that loss of PLD4 affects microglial activation. At P5 and P7, immunostaining for anti-myelin basic protein (MBP) antibody indicated a mild but significant delay in myelination in PLD4-deficient cerebellum. Similar change was also observed in the corpus callosum at P7. However, this difference was not apparent at P10, suggesting that microglial PLD4-deficiency primarily influences the early myelination stage. Thus, microglia may have a transient role in myelination via a PLD4-related mechanism during development.
- Published
- 2016
- Full Text
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