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Article ; Online: Correction to: Astrocytic Extracellular Vesicles Regulated by Microglial Inflammatory Responses Improve Stroke Recovery.

Kijima, Chikage / Inaba, Toshiki / Hira, Kenichiro / Miyamoto, Nobukazu / Yamashiro, Kazuo / Urabe, Takao / Hattori, Nobutaka / Ueno, Yuji

Molecular neurobiology

2023 Volume 61, Issue 2, Page(s) 1022

Language	English
Publishing date	2023-09-20
Publishing country	United States
Document type	Published Erratum
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03657-5
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Article ; Online: Astrocytic Extracellular Vesicles Regulated by Microglial Inflammatory Responses Improve Stroke Recovery.

Kijima, Chikage / Inaba, Toshiki / Hira, Kenichiro / Miyamoto, Nobukazu / Yamashiro, Kazuo / Urabe, Takao / Hattori, Nobutaka / Ueno, Yuji

Molecular neurobiology

2023 Volume 61, Issue 2, Page(s) 1002–1021

Abstract: There are no effective treatments for post-stroke glial scar formation, which inhibits axonal outgrowth and functional recovery after stroke. We investigated whether astrocytic extracellular vesicles (AEVs) regulated by microglia modulate glial scars and ...

Abstract	There are no effective treatments for post-stroke glial scar formation, which inhibits axonal outgrowth and functional recovery after stroke. We investigated whether astrocytic extracellular vesicles (AEVs) regulated by microglia modulate glial scars and improve stroke recovery. We found that peri-infarct glial scars comprised reactive astrocytes with proliferating C3d and decreased S100A10 expression in chronic stroke. In cultured astrocytes, microglia-conditioned media and treatment with P2Y
MeSH term(s)	Rats ; Animals ; Microglia/metabolism ; NF-kappa B/metabolism ; Astrocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Gliosis/pathology ; Stroke/pathology ; Extracellular Vesicles/metabolism
Chemical Substances	NF-kappa B ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2023-09-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03629-9
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Zs.A 2411: Show issues

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Article ; Online: Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.

Jo-Watanabe, Airi / Inaba, Toshiki / Osada, Takahiro / Hashimoto, Ryota / Nishizawa, Tomohiro / Okuno, Toshiaki / Ihara, Sayoko / Touhara, Kazushige / Hattori, Nobutaka / Oh-Hora, Masatsugu / Nureki, Osamu / Yokomizo, Takehiko

Nature communications

2024 Volume 15, Issue 1, Page(s) 1530

Abstract: Homoeostatic regulation of the acid-base balance is essential for cellular functional integrity. However, little is known about the molecular mechanism through which the acid-base balance regulates cellular responses. Here, we report that bicarbonate ... ...

Abstract	Homoeostatic regulation of the acid-base balance is essential for cellular functional integrity. However, little is known about the molecular mechanism through which the acid-base balance regulates cellular responses. Here, we report that bicarbonate ions activate a G protein-coupled receptor (GPCR), i.e., GPR30, which leads to G
MeSH term(s)	Male ; Mice ; Animals ; Bicarbonates ; Calcium/metabolism ; Brain Ischemia ; Receptors, Estrogen/metabolism ; Stroke ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Reperfusion Injury
Chemical Substances	Bicarbonates ; Calcium (SY7Q814VUP) ; Receptors, Estrogen ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45579-3
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Article ; Online: Pleiotropic Effects of Exosomes as a Therapy for Stroke Recovery.

Ueno, Yuji / Hira, Kenichiro / Miyamoto, Nobukazu / Kijima, Chikage / Inaba, Toshiki / Hattori, Nobutaka

International journal of molecular sciences

2020 Volume 21, Issue 18

Abstract: Stroke is the leading cause of disability, and stroke survivors suffer from long-term sequelae even after receiving recombinant tissue plasminogen activator therapy and endovascular intracranial thrombectomy. Increasing evidence suggests that exosomes, ... ...

Abstract	Stroke is the leading cause of disability, and stroke survivors suffer from long-term sequelae even after receiving recombinant tissue plasminogen activator therapy and endovascular intracranial thrombectomy. Increasing evidence suggests that exosomes, nano-sized extracellular membrane vesicles, enhance neurogenesis, angiogenesis, and axonal outgrowth, all the while suppressing inflammatory reactions, thereby enhancing functional recovery after stroke. A systematic literature review to study the association of stroke recovery with exosome therapy was carried out, analyzing species, stroke model, source of exosomes, behavioral analyses, and outcome data, as well as molecular mechanisms. Thirteen studies were included in the present systematic review. In the majority of studies, exosomes derived from mesenchymal stromal cells or stem cells were administered intravenously within 24 h after transient middle cerebral artery occlusion, showing a significant improvement of neurological severity and motor functions. Specific microRNAs and molecules were identified by mechanistic investigations, and their amplification was shown to further enhance therapeutic effects, including neurogenesis, angiogenesis, axonal outgrowth, and synaptogenesis. Overall, this review addresses the current advances in exosome therapy for stroke recovery in preclinical studies, which can hopefully be preparatory steps for the future development of clinical trials involving stroke survivors to improve functional outcomes.
MeSH term(s)	Animals ; Axons/metabolism ; Disease Models, Animal ; Exosomes/metabolism ; Exosomes/transplantation ; Humans ; Mesenchymal Stem Cells/metabolism ; MicroRNAs/metabolism ; Neovascularization, Physiologic ; Neurogenesis ; Stroke/metabolism ; Stroke/therapy ; Synapses/metabolism
Chemical Substances	MicroRNAs
Language	English
Publishing date	2020-09-20
Publishing country	Switzerland
Document type	Journal Article ; Systematic Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21186894
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Article ; Online: Microbial lipopolysaccharide-induced inflammation contributes to cognitive impairment and white matter lesion progression in diet-induced obese mice with chronic cerebral hypoperfusion.

Inaba, Toshiki / Yamashiro, Kazuo / Kurita, Naohide / Ueno, Yuji / Miyamoto, Nobukazu / Hira, Kenichiro / Nakajima, Sho / Kijima, Chikage / Nakaguro, Ryohei / Urabe, Takao / Hattori, Nobutaka

CNS neuroscience & therapeutics

2023 Volume 29 Suppl 1, Page(s) 200–212

Abstract: Aims: White matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia-induced cognitive impairment and WMLs by diet-induced obesity, ... ...

Abstract	Aims: White matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia-induced cognitive impairment and WMLs by diet-induced obesity, including lipopolysaccharide (LPS)-triggered neuroinflammation via toll-like receptor (TLR) 4. Methods: Wild-type (WT) and TLR4-knockout (KO) C57BL/6 mice were fed a high-fat diet (HFD) or low-fat diet (LFD), and subjected to bilateral carotid artery stenosis (BCAS). Diet groups were compared for changes in gut microbiota, intestinal permeability, systemic inflammation, neuroinflammation, WML severity, and cognitive dysfunction. Results: In WT mice, HFD induced obesity and increased cognitive impairment and WML severity compared with LFD-fed mice following BCAS. HFD caused gut dysbiosis and increased intestinal permeability, and plasma LPS and pro-inflammatory cytokine concentrations. Furthermore, HFD-fed mice had higher LPS levels and higher neuroinflammatory status, including increased TLR4 expression, in WMLs. In TLR4-KO mice, HFD also caused obesity and gut dysbiosis but did not increase cognitive impairment or WML severity after BCAS. No difference was found between HFD- and LFD-fed KO mice for LPS levels or inflammatory status in either plasma or WMLs. Conclusion: Inflammation triggered by LPS-TLR4 signaling may mediate obesity-associated exacerbation of cognitive impairment and WMLs from brain ischemia.
MeSH term(s)	Mice ; Animals ; Lipopolysaccharides/toxicity ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism ; Mice, Obese ; Neuroinflammatory Diseases ; White Matter/pathology ; Dysbiosis ; Mice, Inbred C57BL ; Inflammation/metabolism ; Obesity/complications ; Obesity/metabolism ; Cognitive Dysfunction/pathology ; Brain Ischemia/complications ; Brain Ischemia/pathology ; Diet, High-Fat/adverse effects ; Carotid Stenosis/pathology
Chemical Substances	Lipopolysaccharides ; Toll-Like Receptor 4
Language	English
Publishing date	2023-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14301
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Zs.A 4537: Show issues

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Article ; Online: Neuroprotective effects of erythromycin on ischemic injury following permanent focal cerebral ischemia in rats.

Katayama, Yasuo / Inaba, Toshiki / Nito, Chikako / Ueda, Masayuki

Neurological research

2016 Volume 38, Issue 3, Page(s) 275–284

Abstract: Objective: This study aims to determine if erythromycin provides neuroprotective effects against ischemic injury following permanent focal cerebral ischemia.: Methods: Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO). ... ...

Abstract	Objective: This study aims to determine if erythromycin provides neuroprotective effects against ischemic injury following permanent focal cerebral ischemia. Methods: Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO). Each animal received a single subcutaneous injection of erythromycin lactobionate (EM, 50 mg/kg) or vehicle immediately after ischemia. The infarct volume, edema index and neurological performance were evaluated at 24 and 72 h after MCAO. The cerebral blood flow (CBF) was measured with an MRI system at 30 min after MCAO. TUNEL staining and immunohistochemical analyses for oxidative stress (4-HNE, 8-OHdG) and inflammation (Iba-1, TNF-α) in the cortex were conducted at 24 and 72 h after MCAO. Results: The CBF did not differ between the EM-treated and vehicle-treated groups. The EM treatment significantly reduced the infarct volume (p < 0.01) at 24 and 72 h after MCAO and significantly reduced the edema index (p < 0.01) at 24 h. The EM treatment significantly improved the neurological deficit scores (p < 0.05) at 24 and 72 h. EM also significantly suppressed the accumulation of 4-HNE (p < 0.01) and 8-OHdG (p < 0.01) and markedly reduced Iba-1 (p < 0.01) and TNF-α expression (p < 0.05) at both time points. The EM treatment significantly reduced TUNEL-positive cells (p < 0.01) at both time points. Conclusion: These findings suggest that EM can protect against the neuronal damage caused by cerebral ischemia by alleviating inflammation and reducing oxidant stress.
MeSH term(s)	Aldehydes/metabolism ; Animals ; Blood Pressure/drug effects ; Body Temperature/drug effects ; Brain Edema/drug therapy ; Brain Edema/etiology ; Brain Infarction/drug therapy ; Brain Infarction/etiology ; Brain Injuries/diagnostic imaging ; Brain Injuries/drug therapy ; Brain Injuries/etiology ; Calcium-Binding Proteins/metabolism ; Cerebrovascular Circulation/drug effects ; Deoxyguanosine/analogs & derivatives ; Deoxyguanosine/metabolism ; Disease Models, Animal ; Erythromycin/therapeutic use ; In Situ Nick-End Labeling ; Infarction, Middle Cerebral Artery/complications ; Infarction, Middle Cerebral Artery/diagnostic imaging ; Magnetic Resonance Imaging ; Microfilament Proteins/metabolism ; Neuroprotective Agents/therapeutic use ; Rats ; Statistics, Nonparametric ; Time Factors ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Aif1 protein, rat ; Aldehydes ; Calcium-Binding Proteins ; Microfilament Proteins ; Neuroprotective Agents ; Tumor Necrosis Factor-alpha ; Erythromycin (63937KV33D) ; 8-oxo-7-hydrodeoxyguanosine (88847-89-6) ; Deoxyguanosine (G9481N71RO) ; 4-hydroxy-2-nonenal (K1CVM13F96)
Language	English
Publishing date	2016-03
Publishing country	England
Document type	Journal Article
ZDB-ID	424428-x
ISSN	1743-1328 ; 0161-6412
ISSN (online)	1743-1328
ISSN	0161-6412
DOI	10.1080/01616412.2016.1138662
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Zs.A 1491: Show issues

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Article ; Online: Neuroprotective effects of clarithromycin against neuronal damage in cerebral ischemia and in cultured neuronal cells after oxygen-glucose deprivation.

Katayama, Yasuo / Inaba, Toshiki / Nito, Chikako / Suda, Satoshi / Ueda, Masayuki

Life sciences

2017 Volume 168, Page(s) 7–15

Abstract: Aims: Rats subjected to transient focal ischemia and cultured neuronal cells subjected to oxygen-glucose deprivation (OGD) were treated with clarithromycin (CAM) to evaluate the effects of CAM in protecting against neuronal damage.: Main methods: ... ...

Abstract	Aims: Rats subjected to transient focal ischemia and cultured neuronal cells subjected to oxygen-glucose deprivation (OGD) were treated with clarithromycin (CAM) to evaluate the effects of CAM in protecting against neuronal damage. Main methods: Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 90min and then reperfused. Each animal was given an oral dose clarithromycin (CAM, 100mg/kg) or vehicle alone just after the ischemia was commenced. The infarct volume, edema index and neurological performance were assessed after 24 and 72h of reperfusion. The cerebral blood flow (CBF) was measured with an MRI system at 90min after MCAO. After 24 and 72h, oxidative stress (4-HNE, 8-OHdG) and inflammation (Iba-1, TNF-α) were assessed by immunohistochemical analyses and degenerative cells were assessed in the cortex by Fluoro-Jade C (FJC) labeling. The cultured neuronal cells were also used to examine the effects of CAM exposure on the viability of the cells after OGD. Key findings: CBF was unchanged between the two groups. Significant reductions of the infarct volume and edema index, an improved neurological deficit score, a significant suppression of 4-HNE and 8-OHdG expression, marked reductions of Iba-1 and TNF-α expression, and a significant reduction of FJC-positive cells were also observed in the CAM-treated animals at both time points. Treatment with 10μM and 100μM CAM in vitro significantly reduced cell death after OGD. Significance: CAM appears to provide antioxidant and anti-inflammatory effects and protect against neuronal damage after cerebral ischemia and OGD.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Brain/blood supply ; Brain/drug effects ; Brain/pathology ; Brain Ischemia/drug therapy ; Brain Ischemia/pathology ; Cells, Cultured ; Cerebrovascular Circulation/drug effects ; Clarithromycin/pharmacology ; Clarithromycin/therapeutic use ; Glucose/metabolism ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/pathology ; Male ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Oxidative Stress/drug effects ; Oxygen/metabolism ; Rats, Sprague-Dawley
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; Neuroprotective Agents ; Clarithromycin (H1250JIK0A) ; Glucose (IY9XDZ35W2) ; Oxygen (S88TT14065)
Language	English
Publishing date	2017-01-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2016.11.004
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Article ; Online: Neuroprotective effects of pretreatment with macrolide antibiotics on cerebral ischemia reperfusion injury.

Inaba, Toshiki / Katayama, Yasuo / Ueda, Masayuki / Nito, Chikako

Neurological research

2015 Volume 37, Issue 6, Page(s) 514–524

Abstract: Objective: This study aims to determine if macrolide antibiotics have neuroprotective effects against transient cerebral ischemia.: Methods: Sprague-Dawley rats were subjected to cerebral ischemia for 90 minutes followed by 24 or 72 hours of ... ...

Abstract	Objective: This study aims to determine if macrolide antibiotics have neuroprotective effects against transient cerebral ischemia. Methods: Sprague-Dawley rats were subjected to cerebral ischemia for 90 minutes followed by 24 or 72 hours of reperfusion. An oral suspension of roxithromycin (RXM), clarithromycin (CAM), erythromycin (EM), azithromycin (AZM), or kitasamycin (INN) was given at 10 or 100 mg/kg for 7 days before ischemia. The infarct volume, edema volume, and neurological performance were evaluated after 24 and 72 hours of reperfusion. The cerebral blood flow (CBF) was measured with a magnetic resonance imaging (MRI) system after 90 minutes of ischemia. Another experiment was conducted to investigate how the ischemic injury was affected by the interval from the antibiotic pretreatment to the ischemia in rats pretreated with CAM. Results: Roxithromycin, CAM, AZM, and INN significantly reduced the infarct volume in the high-dose group after 24 and 72 hours of reperfusion. All of the agents significantly decreased the edema in the high-dose groups at 24 and 72 hours, while only CAM and AZM significantly reduced the edema volume in the low-dose groups at 24 hours. All of the macrolide antibiotics at the high dose significantly improved neurological deficit scores at 24 and 72 hours. There were no differences in the CBF between the vehicle and respective antibiotic groups. In the experiment examining the interval, the 24-hour interval group exhibited the strongest neuroprotective effect. Discussion: These results demonstrate that the macrolide antibiotics RXM, CAM, EM, AZM, and INN may confer neuroprotective effects against ischemic damage following cerebral ischemia without affecting the CBF.
MeSH term(s)	Animals ; Anti-Bacterial Agents/pharmacology ; Brain/drug effects ; Brain/pathology ; Brain/physiopathology ; Brain Edema/drug therapy ; Brain Edema/pathology ; Brain Edema/physiopathology ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/physiology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Immunohistochemistry ; Ischemic Attack, Transient/drug therapy ; Ischemic Attack, Transient/pathology ; Ischemic Attack, Transient/physiopathology ; Macrolides/pharmacology ; Male ; Neuroprotective Agents/pharmacology ; Random Allocation ; Rats, Sprague-Dawley ; Reperfusion Injury/drug therapy ; Reperfusion Injury/pathology ; Reperfusion Injury/physiopathology ; Time Factors
Chemical Substances	Anti-Bacterial Agents ; Macrolides ; Neuroprotective Agents
Language	English
Publishing date	2015-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	424428-x
ISSN	1743-1328 ; 0161-6412
ISSN (online)	1743-1328
ISSN	0161-6412
DOI	10.1179/1743132815Y.0000000005
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Zs.A 1491: Show issues

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Article ; Online: The effects of A1/A2 astrocytes on oligodendrocyte linage cells against white matter injury under prolonged cerebral hypoperfusion.

Miyamoto, Nobukazu / Magami, Shunsuke / Inaba, Toshiki / Ueno, Yuji / Hira, Kenichiro / Kijima, Chikage / Nakajima, Sho / Yamashiro, Kazuo / Urabe, Takao / Hattori, Nobutaka

Glia

2020 Volume 68, Issue 9, Page(s) 1910–1924

Abstract: As oligodendrocyte precursor cells (OPCs) are vulnerable to ischemia, their differentiation to oligodendrocytes (OLG) is impaired in chronic cerebral hypoperfusion. Astrocyte-OLG interaction is important for white matter homeostasis. Recently, reactive ... ...

Abstract	As oligodendrocyte precursor cells (OPCs) are vulnerable to ischemia, their differentiation to oligodendrocytes (OLG) is impaired in chronic cerebral hypoperfusion. Astrocyte-OLG interaction is important for white matter homeostasis. Recently, reactive astrocytes were separated into two types, A1 (cytotoxic) and A2 (neurotrophic). However, their role in prolonged cerebral hypoperfusion remains unclear. We analyzed the effects of interaction between A1-A2 astrocytes and OPC-OLG under hypoperfusion, focusing on mitochondrial migration. As an in vivo model, chronic hypoperfusion model mice were created by bilateral common carotid artery stenosis (BCAS) using microcoils. As a matching in vitro study, rat primary cells were cocultured with a nonlethal concentration of CoCl
MeSH term(s)	Animals ; Astrocytes ; Brain Ischemia ; Carotid Stenosis ; Culture Media, Conditioned/pharmacology ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; Oligodendroglia ; Rats ; White Matter
Chemical Substances	Culture Media, Conditioned
Language	English
Publishing date	2020-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23814
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Zs.A 2345: Show issues

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Article ; Online: Mucosal-Associated Invariant T Cells Are Involved in Acute Ischemic Stroke by Regulating Neuroinflammation.

Nakajima, Sho / Tanaka, Ryota / Yamashiro, Kazuo / Chiba, Asako / Noto, Daisuke / Inaba, Toshiki / Kurita, Naohide / Miyamoto, Nobukazu / Kuroki, Takuma / Shimura, Hideki / Ueno, Yuji / Urabe, Takao / Miyake, Sachiko / Hattori, Nobutaka

Journal of the American Heart Association

2021 Volume 10, Issue 7, Page(s) e018803

Abstract: Background Mucosal-associated invariant T (MAIT) cells have been associated with inflammation in several autoimmune diseases. However, their relation to ischemic stroke remains unclear. This study attempted to elucidate the role of MAIT cells in acute ... ...

Abstract	Background Mucosal-associated invariant T (MAIT) cells have been associated with inflammation in several autoimmune diseases. However, their relation to ischemic stroke remains unclear. This study attempted to elucidate the role of MAIT cells in acute ischemic stroke in mice. Methods and Results We used MR1 knockout C57BL/6 (MR1
MeSH term(s)	Acute Disease ; Animals ; Disease Models, Animal ; Immunity, Cellular ; Inflammation/immunology ; Ischemic Stroke/immunology ; Ischemic Stroke/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Mucosal-Associated Invariant T Cells/immunology ; Mice
Language	English
Publishing date	2021-03-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.120.018803
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