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Article: LAG-3 expression in microglia regulated by IFN-γ/STAT1 pathway and metalloproteases.

Morisaki, Yuta / Ohshima, Motoki / Suzuki, Hikaru / Misawa, Hidemi

2023 Volume 17, Page(s) 1308972

Abstract: Microglia are resident innate immune cells in the central nervous system (CNS) and play important roles in the development of CNS homeostasis. Excessive activation and neurotoxicity of microglia are observed in several CNS disorders, but the mechanisms ... ...

Abstract	Microglia are resident innate immune cells in the central nervous system (CNS) and play important roles in the development of CNS homeostasis. Excessive activation and neurotoxicity of microglia are observed in several CNS disorders, but the mechanisms regulating their activation remain unclear. Immune checkpoint molecules are expressed on activated immune cells and regulate their activation in peripheral immunity. However, the expression mechanism of immune checkpoint molecules in activated microglia is still unknown. Here, we analyzed the expression of immune checkpoint molecules in activated microglia using the mouse microglial cell line BV2 and primary cultured microglia. The expression of lymphocyte activation gene-3 (LAG-3), a type of immune checkpoint molecule, was increased in microglia activated by IFN-γ. IFN-γ-induced LAG-3 expression in microglia was suppressed by transfection of siRNA targeting STAT1. LAG-3 has two forms, membrane and soluble, and both forms were upregulated in microglia activated by IFN-γ. The production of soluble LAG-3 was suppressed by treatment with inhibitors of metalloproteinases such as ADAM10 and ADAM17. IFN-γ administration into cisterna magna of mice increased LAG-3 expression in spinal microglia. Furthermore, LAG-3 knockdown in microglia promoted nitric oxide production by IFN-γ. Our results demonstrate that LAG-3 expression in microglia is induced by the IFN-γ-STAT1 pathway and soluble LAG-3 production is regulated via cleavage of membranous LAG-3 by metalloproteinases including ADAM10 and ADAM17.
Language	English
Publishing date	2023-11-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1308972
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: [The cognitive decline by aging liver].

Miyake, Yudai / Misawa, Hidemi / Muramatsu, Rieko

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2023 Volume 159, Issue 1, Page(s) 69

MeSH term(s)	Humans ; Aging ; Cognitive Dysfunction/etiology ; Liver ; Cognition
Language	Japanese
Publishing date	2023-11-29
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.23103
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Article: Lysophosphatidic acid stimulates pericyte migration via LPA receptor 1

Yonezu, Yoshino / Tanabe, Shogo / Misawa, Hidemi / Muramatsu, Rieko

Biochemical and biophysical research communications. 2022 Aug. 27, v. 618

2022

Abstract: Lysophosphatidic acid (LPA) is a bioactive compound known to regulate various vascular functions. However, despite the fact that many vascular functions are regulated by peri-vascular cells such as pericytes, the effect of LPA on brain pericytes has not ... ...

Abstract	Lysophosphatidic acid (LPA) is a bioactive compound known to regulate various vascular functions. However, despite the fact that many vascular functions are regulated by peri-vascular cells such as pericytes, the effect of LPA on brain pericytes has not been fully evaluated. Thus, we designed this study to evaluate the effects of LPA on brain pericytes. These experiments revealed that while LPA receptors (LPARs) are expressed in cultured pericytes from mouse brains, LPA treatment does not influence the proliferation of these cells but does have a profound impact on their migration, which is regulated via the expression of LPAR1. LPAR1 expression was also detected in human pericyte culture and LPA treatment of these cells also induced migration. Taken together these findings imply that LPA-LPAR1 signaling is one of the key mechanisms modulating pericyte migration, which may help to control vascular function during development and repair processes.
Keywords	bioactive compounds ; brain ; humans ; lysophospholipids ; mice ; research
Language	English
Dates of publication	2022-0827
Size	p. 61-66.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.06.016
Database	NAL-Catalogue (AGRICOLA)

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Article: [Identification of Wnt7a<sup>K190A</sup> mutant and its restorative action on blood-brain barrier].

Yamagishi, Hiroshi / Yonezu, Yoshino / Misawa, Hidemi / Muramatsu, Rieko

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2022 Volume 157, Issue 6, Page(s) 474

MeSH term(s)	Blood-Brain Barrier ; Biological Transport
Language	Japanese
Publishing date	2022-10-31
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.22093
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Article ; Online: Lysophosphatidic acid stimulates pericyte migration via LPA receptor 1.

Yonezu, Yoshino / Tanabe, Shogo / Misawa, Hidemi / Muramatsu, Rieko

Biochemical and biophysical research communications

2022 Volume 618, Page(s) 61–66

Abstract	Lysophosphatidic acid (LPA) is a bioactive compound known to regulate various vascular functions. However, despite the fact that many vascular functions are regulated by peri-vascular cells such as pericytes, the effect of LPA on brain pericytes has not been fully evaluated. Thus, we designed this study to evaluate the effects of LPA on brain pericytes. These experiments revealed that while LPA receptors (LPARs) are expressed in cultured pericytes from mouse brains, LPA treatment does not influence the proliferation of these cells but does have a profound impact on their migration, which is regulated via the expression of LPAR1. LPAR1 expression was also detected in human pericyte culture and LPA treatment of these cells also induced migration. Taken together these findings imply that LPA-LPAR1 signaling is one of the key mechanisms modulating pericyte migration, which may help to control vascular function during development and repair processes.
MeSH term(s)	Animals ; Cell Movement ; Lysophospholipids/pharmacology ; Mice ; Pericytes/drug effects ; Pericytes/metabolism ; Receptors, Lysophosphatidic Acid/metabolism
Chemical Substances	Lysophospholipids ; Receptors, Lysophosphatidic Acid ; lysophosphatidic acid receptor 1, mouse ; lysophosphatidic acid (PG6M3969SG)
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.06.016
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Article: Depletion of perivascular macrophages delays ALS disease progression by ameliorating blood-spinal cord barrier impairment in SOD1

Adachi, Kazuki / Miyata, Kota / Chida, Yukino / Hirose, Mikako / Morisaki, Yuta / Yamanaka, Koji / Misawa, Hidemi

Frontiers in cellular neuroscience

2023 Volume 17, Page(s) 1291673

Abstract: Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which non-cell-autonomous processes have been proposed as its cause. Non-neuronal cells that constitute the environment around motor neurons are known to mediate the pathogenesis of ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which non-cell-autonomous processes have been proposed as its cause. Non-neuronal cells that constitute the environment around motor neurons are known to mediate the pathogenesis of ALS. Perivascular macrophages (PVM) are immune cells that reside between the blood vessels of the central nervous system and the brain parenchyma; PVM are components of the neurovascular unit and regulate the integrity of the blood-spinal cord barrier (BSCB). However, it is not known whether regulation of BSCB function by PVM is involved in the pathogenesis of ALS. Here, we used SOD1
Language	English
Publishing date	2023-11-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1291673
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Article ; Online: Competitive inhibition of the high-affinity choline transporter by tetrahydropyrimidine anthelmintics.

Okuda, Takashi / Nomura, Yuki / Konishi, Asami / Misawa, Hidemi

European journal of pharmacology

2021 Volume 898, Page(s) 173986

Abstract: The high-affinity choline transporter CHT1 mediates choline uptake, the rate-limiting and regulatory step in acetylcholine synthesis at cholinergic presynaptic terminals. CHT1-medated choline uptake is specifically inhibited by hemicholinium-3, which is ... ...

Abstract	The high-affinity choline transporter CHT1 mediates choline uptake, the rate-limiting and regulatory step in acetylcholine synthesis at cholinergic presynaptic terminals. CHT1-medated choline uptake is specifically inhibited by hemicholinium-3, which is a type of choline analog that acts as a competitive inhibitor. Although the substrate choline and the inhibitor hemicholinium-3 are well-established ligands of CHT1, few potent ligands other than choline analogs have been reported. Here we show that tetrahydropyrimidine anthelmintics, known as nicotinic acetylcholine receptor agonists, act as competitive inhibitors of CHT1. A ligand-dependent trafficking assay in cell lines expressing human CHT1 was designed to search for CHT1 ligands from a collection of biologically active compounds. We found that morantel as well as other tetrahydropyrimidines, pyrantel and oxantel, potently inhibits the high-affinity choline uptake activity of CHT1 in a competitive manner similar to the inhibitor hemicholinium-3. They also inhibit the high-affinity choline transporter from the nematode Caenorhabditis elegans. Finally, tetrahydropyrimidines potently inhibit the high-affinity choline uptake in rat brain synaptosomes at a low micromolar level, resulting in the inhibition of acetylcholine synthesis. The rank order of potency in synaptosomes is as follows: morantel > pyarantel > oxantel (K
MeSH term(s)	Animals ; Anthelmintics/metabolism ; Anthelmintics/pharmacology ; Binding, Competitive ; Biological Transport ; Brain/drug effects ; Brain/metabolism ; Cation Transport Proteins/antagonists & inhibitors ; Cation Transport Proteins/metabolism ; Choline/metabolism ; Female ; HEK293 Cells ; Humans ; Ligands ; Mice ; Morantel/metabolism ; Morantel/pharmacology ; Protein Binding ; Protein Transport ; Pyrantel/analogs & derivatives ; Pyrantel/metabolism ; Pyrantel/pharmacology ; Pyrimidines/metabolism ; Pyrimidines/pharmacology ; Symporters/antagonists & inhibitors ; Symporters/genetics ; Symporters/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism
Chemical Substances	Anthelmintics ; CHT1 protein, rat ; Cation Transport Proteins ; Ligands ; Pyrimidines ; SLC5A7 protein, human ; Symporters ; Pyrantel (4QIH0N49E7) ; Morantel (7NJ031HAX5) ; oxantel (94AJJ30D9E) ; Choline (N91BDP6H0X)
Language	English
Publishing date	2021-02-26
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2021.173986
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Article ; Online: Type selective ablation of postnatal slow and fast fatigue-resistant motor neurons in mice induces late onset kinetic and postural tremor following fiber-type transition and myopathy.

Misawa, Hidemi / Kamishima, Kai / Koyama, Tenkei / Ohgaki, Lisa / Morisaki, Yuta / Yamanaka, Tomoyuki / Itohara, Shigeyoshi / Sawano, Shoko / Mizunoya, Wataru / Ogihara, Naomichi

Experimental neurology

2024 Volume 376, Page(s) 114772

Abstract: Animals on Earth need to hold postures and execute a series of movements under gravity and atmospheric pressure. VAChT-Cre is a transgenic Cre driver mouse line that expresses Cre recombinase selectively in motor neurons of S-type (slow-twitch fatigue- ... ...

Abstract	Animals on Earth need to hold postures and execute a series of movements under gravity and atmospheric pressure. VAChT-Cre is a transgenic Cre driver mouse line that expresses Cre recombinase selectively in motor neurons of S-type (slow-twitch fatigue-resistant) and FR-type (fast-twitch fatigue-resistant). Sequential motor unit recruitment is a fundamental principle for fine and smooth locomotion; smaller-diameter motor neurons (S-type, FR-type) first contract low-intensity oxidative type I and type IIa muscle fibers, and thereafter larger-diameter motor neurons (FInt-type, FF-type) are recruited to contract high-intensity glycolytic type IIx and type IIb muscle fibers. To selectively eliminate S- and FR-type motor neurons, VAChT-Cre mice were crossbred with NSE-DTA mice in which the cytotoxic diphtheria toxin A fragment (DTA) was expressed in Cre-expressing neurons. The VAChT-Cre;NSE-DTA mice were born normally but progressively manifested various characteristics, including body weight loss, kyphosis, kinetic and postural tremor, and muscular atrophy. The progressive kinetic and postural tremor was remarkable from around 20 weeks of age and aggravated. Muscular atrophy was apparent in slow muscles, but not in fast muscles. The increase in motor unit number estimation was detected by electromyography, reflecting compensatory re-innervation by remaining FInt- and FF-type motor neurons to the orphaned slow muscle fibers. The muscle fibers gradually manifested fast/slow hybrid phenotypes, and the remaining FInt-and FF-type motor neurons gradually disappeared. These results suggest selective ablation of S- and FR-type motor neurons induces progressive muscle fiber-type transition, exhaustion of remaining FInt- and FF-type motor neurons, and late-onset kinetic and postural tremor in mice.
MeSH term(s)	Animals ; Motor Neurons/pathology ; Motor Neurons/physiology ; Mice ; Mice, Transgenic ; Tremor/genetics ; Tremor/physiopathology ; Muscle Fibers, Slow-Twitch/pathology ; Muscle Fibers, Fast-Twitch/pathology ; Muscular Diseases/physiopathology ; Muscular Diseases/pathology ; Muscular Diseases/etiology ; Muscle Fatigue/physiology ; Posture/physiology ; Animals, Newborn ; Disease Models, Animal
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2024.114772
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Article: [Motor neuron heterogeneity and selective vulnerability in ALS].

Misawa, Hidemi / Morisaki, Yuta

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2018 Volume 152, Issue 2, Page(s) 64–69

Abstract: Different and selective vulnerability among motor neuron subtypes are a fundamental, but unexplained, feature of amyotrophic lateral sclerosis (ALS): fast-fatigable (FF) motor neurons are the most vulnerable, and fast fatigue-resistant/slow (FR/S) motor ... ...

Abstract	Different and selective vulnerability among motor neuron subtypes are a fundamental, but unexplained, feature of amyotrophic lateral sclerosis (ALS): fast-fatigable (FF) motor neurons are the most vulnerable, and fast fatigue-resistant/slow (FR/S) motor neurons are relatively resistant. We identified that osteopontin (OPN) can serve as a marker of FR/S motor neurons, whereas matrix metalloproteinase-9 (MMP9) is expressed by FF motor neurons in mice. In SOD1
MeSH term(s)	Amyotrophic Lateral Sclerosis ; Animals ; Disease Models, Animal ; Disease Progression ; Mice ; Mice, Transgenic ; Motor Neurons ; Spinal Cord ; Superoxide Dismutase
Chemical Substances	Superoxide Dismutase (EC 1.15.1.1)
Language	Japanese
Publishing date	2018-09-10
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.152.64
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Article: [Modulating lipid metabolism helps axon regeneration].

Yonezu, Yoshino / Misawa, Hidemi / Muramatsu, Rieko

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2020 Volume 155, Issue 5, Page(s) 354

MeSH term(s)	Axons ; Lipid Metabolism ; Nerve Regeneration ; Regeneration
Language	Japanese
Publishing date	2020-09-02
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.20039
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