Rie Hasebe

ORCID: 0000-0003-2009-0595
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About
Contact & Profiles
Research Areas
  • Prion Diseases and Protein Misfolding
  • Trace Elements in Health
  • Herpesvirus Infections and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • RNA regulation and disease
  • Mosquito-borne diseases and control
  • Cytomegalovirus and herpesvirus research
  • Neurological diseases and metabolism
  • Vagus Nerve Stimulation Research
  • Circadian rhythm and melatonin
  • HIV Research and Treatment
  • Viral Infections and Vectors
  • Immune Response and Inflammation
  • Vector-borne infectious diseases
  • Pancreatic and Hepatic Oncology Research
  • Toxin Mechanisms and Immunotoxins
  • Autophagy in Disease and Therapy
  • Reproductive System and Pregnancy
  • Infectious Encephalopathies and Encephalitis
  • Veterinary Oncology Research
  • Monoclonal and Polyclonal Antibodies Research
  • Tryptophan and brain disorders
  • Nicotinic Acetylcholine Receptors Study
  • Immune Cell Function and Interaction
  • Malaria Research and Control

Hokkaido Sapporo Kiyota High School
2025

National Institute for Physiological Sciences
2022-2025

Hokkaido University
2014-2024

National Institutes of Natural Sciences
2022-2023

Tokyo Yamate Medical Center
2023

Institute of Natural Science
2022

Institute of Neuroimmunology of the Slovak Academy of Sciences
2022

National Institute of Allergy and Infectious Diseases
2012

Japan Racing Association
2002

Generation of an abnormal isoform the prion protein (PrP(Sc)) is a key aspect propagation prions. Elucidation intracellular localization PrP(Sc) in prion-infected cells facilitates understanding cellular mechanism propagation. However, technical improvement PrP(Sc)-specific detection required for precise analysis. Here, we show that mAb 132, which recognizes region adjacent to most amyloidogenic PrP, useful by immunofluorescence assay pre-treated with guanidine thiocyanate. Extensive...

10.1099/vir.0.037101-0 article EN Journal of General Virology 2011-11-17

It is well known that anti-prion protein (PrP) monoclonal antibodies (mAbs) inhibit abnormal isoform PrP (PrP Sc ) formation in cell culture. Additionally, passive immunization of anti-PrP mAbs protects the animals from prion infection via peripheral challenge when are administered simultaneously or soon after inoculation. Thus, candidates for treatment diseases. However, effects on disease progression middle and late stages remain unclear. This study carried out intraventricular infusion...

10.1099/vir.0.83578-0 article EN Journal of General Virology 2008-05-12

West Nile virus (WNV) causes viremia after invasion to the hosts by mosquito bite. Endothelial cells could play an important role in WNV spread from blood stream into central nervous system and peripheral tissues. Here, we analyzed capacity of virus-like particles (VLPs) highly virulent NY99 6-LP strain (6-LP VLPs) low virulence Eg101 (Eg cross cultured human endothelial cells. VLPs were transported apical basolateral side cells, whereas Eg hardly transported. The localization tight junction...

10.1186/1471-2180-10-165 article EN cc-by BMC Microbiology 2010-01-01

The endotheliotropism of equine herpesvirus-1 (EHV-1) leads to encephalomyelitis secondary vasculitis and thrombosis in the infected horse central nervous system (CNS). To identify host factors involved EHV-1 infection CNS endothelial cells, we performed functional cloning using an brain microvascular cell cDNA library. Exogenous expression major histocompatibility complex (MHC) class I heavy chain genes conferred susceptibility mouse NIH3T3 which are not naturally susceptible infection....

10.1111/j.1365-2443.2011.01491.x article EN other-oa Genes to Cells 2011-02-10

Neurological diseases caused by encephalitic flaviviruses are severe and associated with high levels of mortality. However, detailed mechanisms viral replication in the brain features pathogenesis remain poorly understood. We carried out a comparative analysis neurotropic flaviviruses: West Nile virus, Japanese encephalitis virus tick-borne (TBEV), primary cultures mouse neurons. All multiplied well neuronal from hippocampus, cerebral cortex cerebellum. The distribution viral-specific...

10.1099/vir.0.061432-0 article EN Journal of General Virology 2014-01-07

ABSTRACT Prion diseases are fatal neurodegenerative disorders characterized by accumulation of PrP Sc , vacuolation neurons and neuropil, astrocytosis, microglial activation. Upregulation gene expressions innate immunity-related factors, including complement factors CD14, is observed in the brains mice infected with prions even early stage infections. When CD14 knockout (CD14 −/− ) were intracerebrally Chandler Obihiro prion strains, survived longer than wild-type (WT) mice, suggesting that...

10.1128/jvi.02072-13 article EN Journal of Virology 2013-10-03

Molecules that inhibit the formation of an abnormal isoform prion protein (PrPSc) in prion-infected cells are candidate therapeutic agents for diseases. Understanding how these molecules PrPSc provides logical basis proper evaluation their potential. In this study, we extensively analyzed effects anti-PrP monoclonal antibody (mAb) 44B1, pentosan polysulfate (PPS), chlorpromazine (CPZ) and U18666A on intracellular dynamics a cellular (PrPC) mouse neuroblastoma to re-evaluate those agents. MAb...

10.1371/journal.pone.0106516 article EN cc-by PLoS ONE 2014-09-02

Neural circuits between lesions are one mechanism through which local inflammation spreads to remote positions. Here, we show the inflammatory signal on side of joint is spread other via sensory neuron–interneuron crosstalk, with ATP at core. Surgical ablation or pharmacological inhibition this neural pathway prevented development side. Mechanistic analysis showed that serves as both a neurotransmitter and an enhancer, thus acting intermediary induces These results suggest blockade pathway,...

10.1084/jem.20212019 article EN cc-by-nc-sa The Journal of Experimental Medicine 2022-05-17

Abstract Neural signaling regulates various reactions in our body including immune responses. Neuromodulation of this using artificial neural activation and/or suppression is a potential treatment diseases and disorders. We here review regulating the system, with special focus on gateway reflex. The reflex novel neuro-immune crosstalk mechanism that tissue-specific inflammatory diseases. have discovered six reflexes so far; all are induced by environmental or stimulations gravity, electrical...

10.1093/intimm/dxaf009 article EN other-oa International Immunology 2025-03-29

ABSTRACT Bone marrow-derived mesenchymal stem cells (MSCs) have been reported to migrate brain lesions in experimental models of ischemia, tumors, and neurodegenerative diseases ameliorate functional deficits. In this study, we attempted evaluate the therapeutic potential MSCs for treating prion diseases. Immortalized human (hMSCs) that express LacZ gene were transplanted into unilateral hippocampi or thalami mice, their distributions monitored by expression β-galactosidase. mice infected...

10.1128/jvi.00165-09 article EN Journal of Virology 2009-03-19

Objectives The central nervous system disorder in systemic lupus erythematosus (SLE), called neuropsychiatric (NPSLE), is one of the most severe phenotypes with various clinical symptoms, including mood disorder, psychosis and delirium as diffuse neuropsychological manifestations (dNPSLE). Although stress aggravating factors for its role pathogenesis dNPSLE remains to be elucidated. We aimed investigate effects on pathophysiology SLE using lupus-prone mice patients’ data. Methods Sleep...

10.1136/ard-2022-222566 article EN Annals of the Rheumatic Diseases 2022-07-11

Trichomonas vaginalis is the most prevalent sexually transmitted parasite worldwide. However, no surveillance system exists to monitor T. cases and drug resistance in Japan.Cervical cytology vaginal swabs were collected from women with without suspected symptoms of infection; these used for detection vaginalis, human papillomavirus (HPV), Candida albicans using specific polymerase chain reaction. Clinical isolates subjected metronidazole susceptibility tests previously reported minimal...

10.1016/j.ijregi.2023.02.007 article EN cc-by-nc-nd IJID Regions 2023-02-28

Abstract It is generally thought that effective treatments for prion diseases need to inhibit propagation, protect neuronal tissues and promote functional recovery of degenerated nerve tissues. In addition, such should be even when given after clinical onset the disease administered via a peripheral route. this study, effect administration an anti‐PrP antibody on progression in prion‐infected mice was examined. mAb 31C6 tail veins at time (120 days post‐inoculation with Chandler strain)...

10.1111/1348-0421.12037 article EN Microbiology and Immunology 2013-04-01

Dupuytren's contracture (DC) is an inflammatory fibrosis characterized by fibroproliferative disorders of the palmar aponeurosis, for which there no effective treatment. Although several genome-wide association studies have identified risk alleles associated with DC, functional linkage between these and pathogenesis remains elusive. We here focused on two single nucleotide polymorphisms (SNPs) rs16879765 rs17171229, in secreted frizzled related protein 4 (SFRP4). investigated SRFP4 IL-6...

10.1093/intimm/dxad004 article EN International Immunology 2023-01-30

Swine hemagglutinating encephalomyelitis virus (HEV) causes or vomiting and wasting disease in suckling piglets. Neurotoropism of the has been demonstrated previous vivo studies. In present study, we investigated infectivity propagation HEV comparison with those pseudorabies (PRV), another neurotropic virus, using dorsal root ganglia cells newborn mice containing nerve non-neuronal cells. infected but did not infect cells, whereas PRV both cell types. By cytoskeletal inhibitors, it was...

10.1292/jvms.71.595 article EN cc-by-nc-nd Journal of Veterinary Medical Science 2009-01-01

Prion diseases are fatal neurodegenerative disorders of humans and animals no effective treatments currently available. Allogenic transplantation immortalized human mesenchymal stem cells (MSCs) can prolong the survival mice infected with prions. However, autologous is an appropriate model for evaluating effects MSCs on prion diseases. Therefore, we isolated purified from femur tibia as compact bone-derived (CB-MSCs). Flow cytometric analysis showed that CB-MSCs were negative myeloid...

10.1099/jgv.0.000907 article EN Journal of General Virology 2017-09-06

In prion diseases, an abnormal isoform of protein (PrPSc) accumulates in neurons, astrocytes, and microglia the brains animals affected by prions. Detailed analyses PrPSc-positive neurons glial cells are required to clarify their pathophysiological roles disease. Here, we report a novel method for detection PrPSc from prion-infected mice flow cytometry using PrPSc-specific staining with monoclonal antibody (MAb) 132. The combination immunolabeling neural cell markers clearly distinguished...

10.1128/jvi.01457-17 article EN Journal of Virology 2017-10-19

The lipopolysaccharides (LPSs) of Rhodobacter are reported to be TLR4 antagonists. Accordingly, the extract azotoformans (RAP99) is used as a health supplement for humans and animals in Japan regulate immune responses vivo . We previously analyzed LPS structure RAP99 (RAP99-LPS) found it different from that E. coli -LPS but similar lipid A sphaeroides (RSLA), known antagonist TLR4, with both having three C14 fatty acyl groups, two C10 phosphates. Here we show RAP99-LPS has an stimulatory...

10.3389/fimmu.2021.675909 article EN cc-by Frontiers in Immunology 2021-05-25

ABSTRACT Although the major component of prion is believed to be oligomer PrP Sc , little information available concerning regions on molecule that affect infectivity. During analysis molecules from various strains, we found Chandler strain showed a unique property in conformational-stability assay, and this appeared useful for studying relationship between Thus, analyzed detail infectivities N-terminally denatured truncated forms proteinase K-resistant PrP. The N-terminal region...

10.1128/jvi.01740-08 article EN Journal of Virology 2009-01-29
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