Misaki Matsumoto

ORCID: 0000-0002-2006-5915
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About
Contact & Profiles
Research Areas
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Pain Mechanisms and Treatments
  • Nitric Oxide and Endothelin Effects
  • Immune Response and Inflammation
  • Liver Disease Diagnosis and Treatment
  • Ion channel regulation and function
  • Adenosine and Purinergic Signaling
  • Liver Disease and Transplantation
  • Liver physiology and pathology
  • Advanced Glycation End Products research
  • Nicotinic Acetylcholine Receptors Study
  • Neuropeptides and Animal Physiology
  • Sphingolipid Metabolism and Signaling
  • Diet, Metabolism, and Disease
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Phytochemical compounds biological activities
  • Peroxisome Proliferator-Activated Receptors
  • Advanced Nanomaterials in Catalysis
  • Phagocytosis and Immune Regulation
  • Hepatitis B Virus Studies
  • Receptor Mechanisms and Signaling
  • Botulinum Toxin and Related Neurological Disorders
  • Molecular Sensors and Ion Detection
  • Cancer Treatment and Pharmacology
  • Neuroscience and Neural Engineering

Kyoto Prefectural University of Medicine
2016-2025

Wakayama Medical University
2024

Kyoto University
2022

Hoshi University
2014-2020

Ebara (Japan)
2018-2020

Institute of Pharmacology
2017

Kyoto Pharmaceutical University
2016

Gunma University
2016

Sapporo Medical University
2013

University of Tsukuba
2013

Paclitaxel (Taxol) is a widely used chemotherapeutic agent in the treatment of several tumors. However, its use often associated with generation peripheral neuropathic pain expressed as mechanical allodynia and thermal hyperalgesia. The molecular mechanism behind this debilitating side effect obscure, efficient drugs for prevention are required. We sought to clarify cellular changes involved nociceptor types underlying paclitaxel-induced test an alleviating gabapentin murine model pain....

10.1124/jpet.106.103614 article EN Journal of Pharmacology and Experimental Therapeutics 2006-05-10

Among multiple isoforms of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase expressed in the liver, phagocytic NOX2 isoform hepatic stellate cells (HSCs) has been demonstrated to play a key role liver fibrogenesis. The aim this study was clarify NOX1, nonphagocytic NADPH oxidase, development fibrosis using Nox1 -deficient mice (Nox1KO). Liver injury and were induced by bile duct ligation (BDL) carbon tetrachloride Nox1KO wildtype littermate (WT). Primary HSCs...

10.1002/hep.24465 article EN Hepatology 2011-05-26

Involvement of reactive oxygen species (ROS) has been suggested in the development psychiatric disorders. NOX1 is a nonphagocytic form NADPH oxidase whose expression nervous system negligible compared with other NOX isoforms. However, NOX1-derived ROS increase inflammatory pain and tolerance to opioid analgesia. To clarify role brain, we examined depressive-like behaviors mice deficient Nox1 ( −/Y ). Depressive-like induced by chronic social defeat stress or administration corticosterone...

10.1523/jneurosci.2988-16.2017 article EN cc-by-nc-sa Journal of Neuroscience 2017-03-17

Clioquinol has been thought of as the causative drug subacute myelo-optic neuropathy (SMON). The underlying mechanisms clioquinol toxicity, however, have not elucidated in detail. Here, we revealed that (20 μm) suppressed expression SCO1 and SCO2 copper chaperones for mitochondrial respiratory chain Complex IV (cytochrome c oxidase) SH-SY5Y neuroblastoma cells. assembly components activity were clioquinol-treated (10-50 decreased cellular ATP levels glucose-free media. induced OMA1...

10.1002/1873-3468.70033 article EN FEBS Letters 2025-03-24

Bradykinin (BK) is well known as a potent mediator of pain and hyperalgesia. Using highly sensitive nociception test, we found that intraplantar (i.pl.) injection BK produced nociceptive hyper-responses in partial sciatic nerve-injured mice, compared with the control sham-operated animals. By use selective agonists antagonists, revealed mice was mediated through B2 receptor, whereas injured B1 receptor. When examined activation extracellular signal-regulated protein kinase (ERK) dorsal root...

10.1124/jpet.103.060335 article EN Journal of Pharmacology and Experimental Therapeutics 2003-11-21

The involvement of reactive oxygen species (ROS) in morphine-induced analgesia and tolerance has been suggested, yet how where ROS take part these processes remains largely unknown. Here, we report a novel role for the superoxide-generating enzyme NOX1/NADPH oxidase regulation acute analgesic tolerance. In mice lacking Nox1 ( −/ Y ), magnitude induced by morphine was significantly augmented. More importantly, repeated administration suppressed compared with that littermates, wild-type +/ ....

10.1523/jneurosci.4136-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-12-07

Accumulating evidence suggests that reactive oxygen species (ROS) generated by endogenous metabolic enzymes are involved in a variety of intracellular mechanisms. In particular, superoxide-generating NADPH oxidase (Nox) 1 is highly expressed the colon and has been implicated physiological pathophysiological states tissues. However, its role tissue repair following colitis not fully elucidated. Our study using experimental mice showed mucosal layer did occur Nox1-deficient dextran sulfate...

10.1538/expanim.15-0127 article EN EXPERIMENTAL ANIMALS 2016-01-01

Lysophosphatidic acid is a bioactive lipid mediator with neuronal activities. We previously reported crucial role for lysophosphatidic 1 receptor-mediated signaling in neuropathic pain mechanisms. Intrathecal administration of (1 nmol) induced abnormal behaviors, such as thermal hyperalgesia, mechanical allodynia, A-fiber hypersensitization, and C-fiber hyposensitization, all which were also observed partial sciatic nerve injury-induced pain. Ki-16425 (30 mg/kg, i.p.), receptor antagonist,...

10.1111/j.1471-4159.2009.05987.x article EN Journal of Neurochemistry 2009-02-14

Background: We have previously demonstrated that different spinal transmissions are involved in the nociceptive behavior caused by electrical stimulation of Aβ-, Aδ- or C-fibers using a Neurometer® naïve mice. In this study, we attempted to pharmacologically characterize alteration transmission induced partial sciatic nerve injury terms and phosphorylation extracellular signal-regulated kinase (pERK) dorsal horn. Results: Aβ-fiber responses (2000-Hz), which were selectively blocked...

10.1186/1744-8069-4-25 article EN cc-by-nc Molecular Pain 2008-01-01

Involvement of reactive oxygen species derived from nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase has been documented in the development hypoxia-induced model pulmonary arterial hypertension (PAH). Because PAH-like phenotype was demonstrated mice deficient Nox1 gene (Nox1(-/Y)) raised under normoxia, aim this study to clarify how lack NOX1/NADPH could lead pathology.Spontaneous enlargement and hypertrophy right ventricle, accompanied by vessels, were Nox1(-/Y) 9...

10.1161/atvbaha.113.302107 article EN Arteriosclerosis Thrombosis and Vascular Biology 2013-11-15

Background: We have proposed that nerve injury-specific loss of spinal tonic cholinergic inhibition may play a role in the analgesic effects nicotinic acetylcholine receptor (nAChR) agonists on neuropathic pain. However, pain remains to be well characterized. Results: Here, we show choline acetyltransferase (ChAT) signals were localized not only outer dorsal horn fibers (lamina I–III) and motor neurons cord, but also vast majority root ganglion (DRG). When mice treated with an antisense...

10.1186/1744-8069-3-41 article EN cc-by-nc Molecular Pain 2007-01-01

Lysophosphatidic acid receptor subtype LPA 1 is crucial for the initiation of neuropathic pain and underlying changes, such as up-regulation Ca 2 + channel α δ-1 subunit in dorsal root ganglia (DRG), PKCγ spinal horn, demyelination fibers. In present study, we further examined involvement signaling reorganization Aβ-fiber-mediated transmission, which presumed to underlie allodynia. Following nerve injury, phosphorylation extracellular-signal regulated kinase (pERK) by Aβ-fiber stimulation...

10.1186/1744-8069-4-46 article EN cc-by-nc Molecular Pain 2008-01-01

EROS (essential for reactive oxygen species) protein is indispensable expression of gp91 phox , the catalytic core phagocyte NADPH oxidase. deficiency in humans a novel cause severe immunodeficiency, chronic granulomatous disease, but its mechanism action was unknown until now. We elucidate role EROS, showing it acts at earliest stages maturation. It binds immature 58 kDa directly, preventing degradation and allowing glycosylation via oligosaccharyltransferase machinery incorporation heme...

10.7554/elife.76387 article EN cc-by eLife 2022-11-24

In the present study, we first report an in vivo characterization of flexor responses induced by three distinct sine-wave stimuli electrical stimulation-induced paw flexion (EPF) test mice. The fixed electric stimulations 5 Hz (C-fiber), 250 (Aδ-fiber) and 2000 (Aβ-fiber) to hind mice a paw-flexion response vocalization. average threshold for was much lower than that Neonatally (P3) pretreatment with capsaicin degenerate polymodal substance P-ergic C-fiber neurons increased (C-fiber)...

10.1186/1744-8069-2-16 article EN cc-by-nc Molecular Pain 2006-01-01

NOX is the catalytic subunit of NADPH oxidase, superoxide-generating enzyme. Among several isoforms NOX, NOX4 abundantly expressed in various tissues. To clarify mechanisms constitutive and ubiquitous expression NOX4, promoter activities human gene were analyzed by reporter assays. The 5'-flanking non-coding regions are known to contain multiple GC bases. them, three GC-boxes containing putative Sp/Klf-binding sites, which not found rodent genes, suggested be essential for basal SH-SY5Y...

10.1111/j.1742-4658.2011.08018.x article EN FEBS Journal 2011-01-14

NOX1/NADPH oxidase, a nonphagocytic isoform of reactive oxygen species–producing enzymes, is highly expressed in the colon, but physiologic and pathophysiologic roles this are not fully understood. The present study investigated role NOX1 development colonic inflammation trinitrobenzene sulfonic acid (TNBS)-induced murine colitis model. Intrarectal injection TNBS caused severe accompanied by body weight loss, diarrhea, increased myeloperoxidase (MPO) activity wild-type (WT) mice. In...

10.1124/jpet.116.235580 article EN Journal of Pharmacology and Experimental Therapeutics 2016-10-17
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