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3. Quantitative measurement of peritumoral concentrations of glutamate, N-acetyl aspartate, and lactate on magnetic resonance spectroscopy predicts glioblastoma-related refractory epilepsy

Author

Nakamura, Yawara, Inoue, Akihiro, Nishikawa, Masahiro, Ohnishi, Takanori, Yano, Hajime, Kanemura, Yonehiro, Ohtsuka, Yoshihiro, Ozaki, Saya, Kusakabe, Kosuke, Suehiro, Satoshi, Yamashita, Daisuke, Shigekawa, Seiji, Watanabe, Hideaki, Kitazawa, Riko, Tanaka, Junya, and Kunieda, Takeharu

Published
2022
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9. Prediction of Glioma Stemlike Cell Infiltration in the Non–Contrast-Enhancing Area by Quantitative Measurement of Lactate on Magnetic Resonance Spectroscopy in Glioblastoma

Author

Inoue, Akihiro, Nishikawa, Masahiro, Ohnishi, Takanori, Yano, Hajime, Kanemura, Yonehiro, Ohtsuka, Yoshihiro, Ozaki, Saya, Nakamura, Yawara, Matsumoto, Shirabe, Suehiro, Satoshi, Yamashita, Daisuke, Shigekawa, Seiji, Watanabe, Hideaki, Kitazawa, Riko, Tanaka, Junya, and Kunieda, Takeharu

Published
2021
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11. Chloride intracellular channel protein 2 is secreted and inhibits MMP14 activity, while preventing tumor cell invasion and metastasis

Author

Ozaki, Saya, Umakoshi, Akihiro, Yano, Hajime, Ohsumi, Shota, Sumida, Yutaro, Hayase, Erika, Usa, Eika, Islam, Afsana, Choudhury, Mohammed E., Nishi, Yusuke, Yamashita, Daisuke, Ohtsuka, Yoshihiro, Nishikawa, Masahiro, Inoue, Akihiro, Suehiro, Satoshi, Kuwabara, Jun, Watanabe, Hideaki, Takada, Yasutsugu, Watanabe, Yuji, Nakano, Ichiro, Kunieda, Takeharu, and Tanaka, Junya

Published
2021
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36. Enhancement of Thermoelectric Properties of n-Type Bi2Te3–xSex by Energy Filtering Effect

Author

Ken Kurosaki, Masaya Kumagai, Tanaka Junya, Yuhei Kawajiri, Yuji Ohishi, Sora-at Tanusilp, and Manabu Ishimaru

Subjects
Materials science, Condensed matter physics, Thermoelectric effect, Materials Chemistry, Electrochemistry, Energy Engineering and Power Technology, Chemical Engineering (miscellaneous), Electrical and Electronic Engineering, Energy (signal processing)
Published
2021
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37. A Narrative Review on CD44's Role in Glioblastoma Invasion, Proliferation, and Tumor Recurrence.

Author

Inoue, Akihiro, Ohnishi, Takanori, Nishikawa, Masahiro, Ohtsuka, Yoshihiro, Kusakabe, Kosuke, Yano, Hajime, Tanaka, Junya, and Kunieda, Takeharu

Subjects
PROTEINS, CANCER invasiveness, CELL receptors, GLIOMAS, CANCER relapse, GENE expression, CELLULAR signal transduction, STEM cells, CELL proliferation, GENES, DESCRIPTIVE statistics, REACTIVE oxygen species, VASCULAR endothelial growth factors, OXYGEN in the body
Abstract

Simple Summary: As recurrence in glioblastoma is locally generated around the resection cavity, surviving glioma stem-like cells may cause recurrence. Glioma stem-like cells expressing high levels of CD44 are highly invasive and are required to change to less invasive, more proliferative types to generate a recurrent tumor. CD44 promotes both the invasion and proliferation of tumor cells via various signaling pathways. Among these, paired pathways show reciprocal activation of invasion and proliferation under different conditions of oxygenation. Severe hypoxia activates genes related to cell invasion, whereas moderate hypoxia activates genes related to cell proliferation. CD44 is associated with both pathways and plays a critical role in regulating the balance between the promotion of cell invasion and cell proliferation. These results may indicate that CD44 is a key molecule for executing tumor recurrence in glioblastoma. High invasiveness is a characteristic of glioblastoma (GBM), making radical resection almost impossible, and thus, resulting in a tumor with inevitable recurrence. GBM recurrence may be caused by glioma stem-like cells (GSCs) that survive many kinds of therapy. GSCs with high expression levels of CD44 are highly invasive and resistant to radio-chemotherapy. CD44 is a multifunctional molecule that promotes the invasion and proliferation of tumor cells via various signaling pathways. Among these, paired pathways reciprocally activate invasion and proliferation under different hypoxic conditions. Severe hypoxia (0.5–2.5% O2) upregulates hypoxia-inducible factor (HIF)-1α, which then activates target genes, including CD44, TGF-β, and cMET, all of which are related to tumor migration and invasion. In contrast, moderate hypoxia (2.5–5% O2) upregulates HIF-2α, which activates target genes, such as vascular endothelial growth factor (VEGF)/VEGFR2, cMYC, and cyclin D1. All these genes are related to tumor proliferation. Oxygen environments around GBM can change before and after tumor resection. Before resection, the oxygen concentration at the tumor periphery is severely hypoxic. In the reparative stage after resection, the resection cavity shows moderate hypoxia. These observations suggest that upregulated CD44 under severe hypoxia may promote the migration and invasion of tumor cells. Conversely, when tumor resection leads to moderate hypoxia, upregulated HIF-2α activates HIF-2α target genes. The phenotypic transition regulated by CD44, leading to a dichotomy between invasion and proliferation according to hypoxic conditions, may play a crucial role in GBM recurrence. [ABSTRACT FROM AUTHOR]

Published
2023
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38. Identification of CD44 as a Reliable Biomarker for Glioblastoma Invasion: Based on Magnetic Resonance Imaging and Spectroscopic Analysis of 5-Aminolevulinic Acid Fluorescence.

Author

Inoue, Akihiro, Ohnishi, Takanori, Nishikawa, Masahiro, Watanabe, Hideaki, Kusakabe, Kosuke, Taniwaki, Mashio, Yano, Hajime, Ohtsuka, Yoshihiro, Matsumoto, Shirabe, Suehiro, Satoshi, Yamashita, Daisuke, Shigekawa, Seiji, Takahashi, Hisaaki, Kitazawa, Riko, Tanaka, Junya, and Kunieda, Takeharu

Subjects
MAGNETIC resonance imaging, SPECTROSCOPIC imaging, CD44 antigen, IMAGE analysis, ACID analysis, METHYLGUANINE
Abstract

Recurrent glioblastoma multiforme (GBM) is largely attributed to peritumoral infiltration of tumor cells. As higher CD44 expression in the tumor periphery correlates with higher risk of GBM invasion, the present study analyzed the relationship between CD44 expression and magnetic resonance imaging (MRI)-based invasiveness of GBM on a large scale. We also quantitatively evaluated GBM invasion using 5-aminolevulinic acid (5-ALA) spectroscopy to investigate the relationship between CD44 expression and tumor invasiveness as evaluated by intraoperative 5-ALA intensity. Based on MRI, GBM was classified as high-invasive type in 28 patients and low-invasive type in 22 patients. High-invasive type expressed CD44 at a significantly higher level than low-invasive type and was associated with worse survival. To quantitatively analyze GBM invasiveness, the relationship between tumor density in the peritumoral area and the spectroscopic intensity of 5-ALA was investigated. Spectroscopy showed that the 5-ALA intensity of infiltrating tumor cells correlated with tumor density as represented by the Ki-67 staining index. No significant correlation between CD44 and degree of 5-ALA-based invasiveness of GBM was found, but invasiveness of GBM as evaluated by 5-ALA matched the classification from MRI in all except one case, indicating that CD44 expression at the GBM periphery could provide a reliable biomarker for invasiveness in GBM. [ABSTRACT FROM AUTHOR]

Published
2023
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39. The anti-inflammatory and anti-oxidative effect of a classical hypnotic bromovalerylurea mediated by the activation of NRF2.

Author

Takeda, Haruna, Nakajima, Yoshihiro, Yamaguchi, Teruaki, Watanabe, Itaru, Miyoshi, Shoko, Nagashio, Kodai, Sekine, Hiroki, Motohashi, Hozumi, Yano, Hajime, and Tanaka, Junya

Subjects
NUCLEAR factor E2 related factor, HYPNOTICS
Abstract

The Kelch-like ECH-associated protein 1–nuclear factor erythroid 2-related factor 2 (KEAP1–NRF2) system plays a central role in redox homeostasis and inflammation control. Oxidative stress or electrophilic compounds promote NRF2 stabilization and transcriptional activity by negatively regulating its inhibitor, KEAP1. We have previously reported that bromovalerylurea (BU), originally developed as a hypnotic, exerts anti-inflammatory effects in various inflammatory disease models. However, the molecular mechanism underlying its effect remains uncertain. Herein, we found that by real-time multicolor luciferase assay using stable luciferase red3 (SLR3) and green-emitting emerald luciferase (ELuc), BU potentiates NRF2-dependent transcription in the human hepatoblastoma cell line HepG2 cells, which lasted for more than 60 h. Further analysis revealed that BU promotes NRF2 accumulation and the transcription of its downstream cytoprotective genes in the HepG2 and the murine microglial cell line BV2. Keap1 knockdown did not further enhance NRF2 activity, suggesting that BU upregulates NRF2 by targeting KEAP1. Knockdown of Nfe2l2 in BV2 cells diminished the suppressive effects of BU on the production of pro-inflammatory mediators, like nitric oxide (NO) and its synthase NOS2, indicating the involvement of NRF2 in the anti-inflammatory effects of BU. These data collectively suggest that BU could be repurposed as a novel NRF2 activator to control inflammation and oxidative stress. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Chloride Intracellular Channel Protein 2 Promotes Microglial Invasion: A Link to Microgliosis in the Parkinson's Disease Brain.

Author

Choudhury, Mohammed E., Ozaki, Saya, Miyaue, Noriyuki, Matsuura, Taisei, Mikami, Kanta, Islam, Afsana, Kubo, Madoka, Ando, Rina, Yano, Hajime, Kunieda, Takeharu, Nagai, Masahiro, and Tanaka, Junya

Subjects
PARKINSON'S disease, CHLORIDE channels, BRAIN diseases, MICROGLIA, RECOMBINANT proteins
Abstract

Activated microglia potentially cause neurodegeneration in Parkinson's disease (PD). Matrix metalloproteinase (MMP)-9 plays a crucial role in the pathogenesis of PD, but the modulator of microglial release of MMP-9 remains obscure. Given the modulatory effect of chloride intracellular channel protein 2 (CLIC2) on MMPs, we aimed to determine the role of CLIC2 in regulating microglial MMP expression and activation. We found that CLIC2 is expressed in microglia and neurons in rat brain tissue and focused on the function of CLIC2 in primary cultured microglia. Exposure to recombinant CLIC2 protein enhanced microglial invasion activity, and its knockdown abolished this activity. Moreover, increased activation of MMP-9 was confirmed by the addition of the CLIC2 protein, and CLIC2 knockdown eliminated this activation. Additionally, increased expression of CLIC2 was observed in PD-modeled tissue. In conclusion, CLIC2 increases MMP-9 activity in the microglia, which are involved in PD pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Surgical stress quickly affects the numbers of circulating B-cells and neutrophils in murine septic and aseptic models through a β2 adrenergic receptor.

Author

Nishioka, Ryutaro, Nishi, Yusuke, Choudhury, Mohammed E., Miyaike, Riko, Shinnishi, Ayataka, Umakoshi, Kensuke, Takada, Yasutsugu, Sato, Norio, Aibiki, Mayuki, Yano, Hajime, and Tanaka, Junya

Subjects
ADRENERGIC receptors, ADRENERGIC agonists, B cells, SYMPATHETIC nervous system, MYELOID cells, BETA adrenoceptors, ALPHA adrenoceptors
Abstract

Sepsis is a pathology accompanied by increases in myeloid cells and decreases in lymphoid cells in circulation. In a murine sepsis model induced by cecum ligation and puncture (CLP), increasing numbers of neutrophils and decreasing levels of B-cells in circulation are among the earliest changes in the immune system. However, to date, the mechanisms for these changes remain to be elucidated. The study here sought to elucidate mechanisms underlying the changes in the leukocyte levels after CLP and also to determine what, if any, role for an involvement of the sympathetic nervous system (SNS). Here, male C57/BL6 mice were subjected to CLP or sham-CLP (abdominal wall incised, but cecum was not punctured). The changes in the number of circulating leukocytes over time were then investigated using flow cytometry. The results showed that a sham-CLP led to increased polymorphonuclear cells (PMN; most of which are neutrophils) and decreased B-cells in the circulation to an extent similar to that induced by CLP. Effects of adrenergic agonists and antagonists, as well as of adrenalectomy, were also examined in mice that underwent CLP or sham-CLP. Administering adrenaline or a β2 adrenergic receptor agonist (clenbuterol) to mice 3 h before sacrifice produced almost identical changes to as what was seen 2 h after performing a sham-CLP. In contrast, giving a β2 adrenergic receptor antagonist ICI118,551 1 h before a CLP or sham-CLP suppressed the expected changes 2 h after the operations. Noradrenaline and an α1 adrenergic receptor agonist phenylephrine did not exert significant effects. Adrenalectomy 24 h before a sham-CLP significantly abolished the expected sham-CLP-induced changes seen earlier. Clenbuterol increased splenocyte expression of Cxcr4 (a chemokine receptor gene); adrenalectomy abolished sham-CLP-induced Cxcr4 expression. A CXCR4 antagonist AMD3100 repressed the sham-CLP-induced changes. From these results, it may be concluded that sepsis-induced activation of the SNS may be one cause for immune dysfunction in sepsis – regardless of the pathogenetic processes. [ABSTRACT FROM AUTHOR]

Published
2022
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