Faculty Profiles - ASANUMA Masato

Papers - ASANUMA Masato

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Cerebellar Blood Flow and Gene Expression in Crossed Cerebellar Diaschisis after Transient Middle Cerebral Artery Occlusion in Rats Reviewed

Naoya Kidani, Tomohito Hishikawa, Masafumi Hiramatsu, Shingo Nishihiro, Kyohei Kin, Yu Takahashi, Satoshi Murai, Kenji Sugiu, Takao Yasuhara, Ikuko Miyazaki, Masato Asanuma, Isao Date

International Journal of Molecular Sciences 21 ( 11 ) 4137 - 4137 2020.6

Language：English Publishing type：Research paper (scientific journal) Publisher：MDPI AG

Crossed cerebellar diaschisis (CCD) is a state of hypoperfusion and hypometabolism in the contralesional cerebellar hemisphere caused by a supratentorial lesion, but its pathophysiology is not fully understood. We evaluated chronological changes in cerebellar blood flow (CbBF) and gene expressions in the cerebellum using a rat model of transient middle cerebral artery occlusion (MCAO). CbBF was analyzed at two and seven days after MCAO using single photon emission computed tomography (SPECT). DNA microarray analysis and western blotting of the cerebellar cortex were performed and apoptotic cells in the cerebellar cortex were stained. CbBF in the contralesional hemisphere was significantly decreased and this lateral imbalance recovered over one week. Gene set enrichment analysis revealed that a gene set for “oxidative phosphorylation” was significantly upregulated while fourteen other gene sets including “apoptosis”, “hypoxia” and “reactive oxygen species” showed a tendency toward upregulation in the contralesional cerebellum. MCAO upregulated the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the contralesional cerebellar cortex. The number of apoptotic cells increased in the molecular layer of the contralesional cerebellum. Focal cerebral ischemia in our rat MCAO model caused CCD along with enhanced expression of genes related to oxidative stress and apoptosis.

DOI： 10.3390/ijms21114137

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Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson’s Disease Reviewed

Ikuko Miyazaki, Nami Isooka, Fuminori Imafuku, Jin Sun, Ryo Kikuoka, Chieko Furukawa, Masato Asanuma

International Journal of Molecular Sciences 21 ( 9 ) 3254 - 3254 2020.5

Authorship：Last author Language：English Publishing type：Research paper (scientific journal) Publisher：MDPI AG

Epidemiological studies demonstrated that pesticide exposure, such as rotenone and paraquat, increases the risk of Parkinson’s disease (PD). Chronic systemic exposure to rotenone, a mitochondrial complex I inhibitor, could reproduce many features of PD. However, the adoption of the models is limiting because of variability in animal sensitivity and the inability of other investigators to consistently reproduce the PD neuropathology. In addition, most of rotenone models were produced in rats. Here, we tried to establish a high-reproducible rotenone model using C57BL/6J mice. The rotenone mouse model was produced by chronic systemic exposure to a low dose of rotenone (2.5 mg/kg/day) for 4 weeks by subcutaneous implantation of rotenone-filled osmotic mini pump. The rotenone-treated mice exhibited motor deficits assessed by open field, rotarod and cylinder test and gastrointestinal dysfunction. Rotenone treatment decreased the number of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) and lesioned nerve terminal in the striatum. In addition, we observed significant reduction of cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and the intestinal myenteric plexus. Moreover, α-synuclein was accumulated in neuronal soma in the SNpc, DMV and intestinal myenteric plexus in rotenone-treated mice. These data suggest that the low-dose rotenone mouse model could reproduce behavioral and central and peripheral neurodegenerative features of PD and be a useful model for investigation of PD pathogenesis.

DOI： 10.3390/ijms21093254

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Effects of maternal bisphenol A diglycidyl ether exposure during gestation and lactation on behavior and brain development of the offspring Reviewed

Ikuko Miyazaki, Ryo Kikuoka, Nami Isooka, Mika Takeshima, Kanau Sonobe, Rei Arai, Hidemaru Funakoshi, Kyle E. Quin, Jonathan Smart, Kazumasa Zensho, Masato Asanuma

Food and Chemical Toxicology 138 111235 - 111235 2020.4

Dopaminergic neuroprotective effects of rotigotine via 5-HT1A receptors: Possibly involvement of metallothionein expression in astrocytes Reviewed

Nami Isooka, Ikuko Miyazaki, Ryo Kikuoka, Kouichi Wada, Erika Nakayama, Kotaro Shin, Daichi Yamamoto, Yoshihisa Kitamura, Masato Asanuma

Neurochemistry International 132 104608 - 104608 2020.1

Attenuation of Macrophage Migration Inhibitory Factor-Stimulated Signaling via S-Nitrosylation Reviewed

Kengo Nakahara, Kana Fujikawa, Hideki Hiraoka, Ikuko Miyazaki, Masato Asanuma, Akihiro Ito, Nobumasa Takasugi, Takashi Uehara

Biological and Pharmaceutical Bulletin 42 ( 6 ) 1044 - 1047 2019.6

Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice Reviewed

Ikuko Miyazaki, Nami Isooka, Kouichi Wada, Ryo Kikuoka, Yoshihisa Kitamura, Masato Asanuma

Cells 8 ( 3 ) 221 - 221 2019.3

Authorship：Last author Language：English Publishing type：Research paper (scientific journal) Publisher：MDPI AG

Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian models, because the toxin induces PD-like pathology. Here, we examined the neuroprotective effects of CA and CGA against the rotenone-induced degeneration of central dopaminergic and peripheral enteric neurons. Male C57BL/6J mice were chronically administered rotenone (2.5 mg/kg/day), subcutaneously for four weeks. The animals were orally administered CA or CGA daily for 1 week before rotenone exposure and during the four weeks of rotenone treatment. Administrations of CA or CGA prevented rotenone-induced neurodegeneration of both nigral dopaminergic and intestinal enteric neurons. CA and CGA upregulated the antioxidative molecules, metallothionein (MT)-1,2, in striatal astrocytes of rotenone-injected mice. Primary cultured mesencephalic or enteric cells were pretreated with CA or CGA for 24 h, and then further co-treated with a low dose of rotenone (1–5 nM) for 48 h. The neuroprotective effects and MT upregulation induced by CA and CGA in vivo were reproduced in cultured cells. Our data indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus.

DOI： 10.3390/cells8030221

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Region-Specific Neuroprotective Features of Astrocytes against Oxidative Stress Induced by 6-Hydroxydopamine Reviewed

Masato Asanuma, Nao Okumura-Torigoe, Ikuko Miyazaki, Shinki Murakami, Yoshihisa Kitamura, Toshiaki Sendo

International Journal of Molecular Sciences 20 ( 3 ) 598 - 598 2019.1

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：MDPI AG

In previous studies, we found regional differences in the induction of antioxidative molecules in astrocytes against oxidative stress, postulating that region-specific features of astrocytes lead region-specific vulnerability of neurons. We examined region-specific astrocytic features against dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) as an oxidative stress using co-culture of mesencephalic neurons and mesencephalic or striatal astrocytes in the present study. The 6-OHDA-induced reduction of mesencephalic dopamine neurons was inhibited by co-culturing with astrocytes. The co-culture of midbrain neurons with striatal astrocytes was more resistant to 6-OHDA than that with mesencephalic astrocytes. Furthermore, glia conditioned medium from 6-OHDA-treated striatal astrocytes showed a greater protective effect on the 6-OHDA-induced neurotoxicity and oxidative stress than that from mesencephalic astrocytes. The cDNA microarray analysis showed that the number of altered genes in both mesencephalic and striatal astrocytes was fewer than that changed in either astrocyte. The 6-OHDA treatment, apparently up-regulated expressions of Nrf2 and some anti-oxidative or Nrf2-regulating phase II, III detoxifying molecules related to glutathione synthesis and export in the striatal astrocytes but not mesencephalic astrocytes. There is a profound regional difference of gene expression in astrocytes induced by 6-OHDA. These results suggest that protective features of astrocytes against oxidative stress are more prominent in striatal astrocytes, possibly by secreting humoral factors in striatal astrocytes.

DOI： 10.3390/ijms20030598

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Involvement of 5-HT2A receptor hyperfunction in the anxiety-like behavior induced by doxorubicin and cyclophosphamide combination treatment in rats Reviewed

Yuka Nakamura, Yoshihisa Kitamura, Yusuke Sumiyoshi, Nanami Naito, Shiho Kan, Soichiro Ushio, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

Journal of Pharmacological Sciences 138 ( 3 ) 192 - 197 2018.11

Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

We examined whether combination treatment with doxorubicin and cyclophosphamide, a traditional chemotherapy for breast cancer, induced anxiety-like behavior in rats. Furthermore, we evaluated the role of the serotonin (5-HT)2A receptor subtype in the anxiety-like behavior induced by such chemotherapy. Rats were intraperitoneally injected with doxorubicin and cyclophosphamide once a week for 2 weeks. This caused the rats to display anxiety-like behavior during the light-dark test. In addition, we examined the rats' 5-HT2A receptor-mediated behavioral responses. Combination treatment with doxorubicin and cyclophosphamide significantly increased (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, (a 5-HT2A receptor agonist)-induced wet-dog shake activity. This anxiety-like behavior was significantly inhibited by mirtazapine, a 5-HT2A receptor antagonist/5-HT1A receptor agonist, and tandospirone, a partial 5-HT1A receptor agonist, but not by fluoxetine, a selective serotonin reuptake inhibitor. The anxiety-like behavior induced by doxorubicin and cyclophosphamide combination treatment is mediated by hyperfunctioning of the 5-HT2A receptor. Thus, 5-HT2A receptor antagonists or 5-HT1A receptor agonists might be useful for treating chemotherapy-induced anxiety disorders.

DOI： 10.1016/j.jphs.2018.10.001

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Application of Single Prolonged Stress Induces Post-traumatic Stress Disorder-like Characteristics in Mice. Reviewed

Ken-Ichi Tanaka, Takao Yagi, Takeshi Nanba, Masato Asanuma

Acta Medica Okayama 72 ( 5 ) 479 - 485 2018.10

Authorship：Last author Language：English Publishing type：Research paper (scientific journal)

© 2018, by Okayama University Medical School. We tried to clarify the applicability of a single prolonged stress (SPS) protocol as post-traumatic stress disorder (PTSD) model in mice. To investigate PTSD pathophysiology, we conducted hypothalamo-pituitary-adrenal (HPA) negative feedback testing at 1, 4, 8 and 12 weeks after the SPS by administrating a dexamethasone (DEX) suppression test. The SPS induced over-suppression of the HPA system by DEX treatment at 8 and 12 weeks. To investigate PTSD-like behavioral characteristics, we subjected mice to testing in a light/dark box (to assess anxiety), a Y-maze (working memory), a cliff avoidance (visual cognition), and an open field (locomotor activity) at 1, 4, 8 and 12 weeks after the SPS. In the light/dark box test, the SPS-applied mice spent significantly less time in the light box at 8 or 12 weeks. In the cliff avoidance test, the SPS-applied mice spent significantly less time in the open area at 1 week. However, in both the Y-maze test and the open field test, SPS-applied mice tended toward slight decreases in a time-dependent manner until 12 weeks. Therefore, SPS-applied mice may thus be useful for assessing characteristics relevant to PTSD that coincide with changes in the HPA axis.

DOI： 10.18926/AMO/56245

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Neuroprotective effect of fermented papaya preparation by activation of Nrf2 pathway in astrocytes Reviewed

Shinki Murakami, Ikuko Miyazaki, Masato Asanuma

Nutritional Neuroscience 21 ( 3 ) 176 - 184 2018.3

Effect of alteration of glutathione content on cell viability in a-synuclein-transfected SH-SY5Y cells. Reviewed

Ken-ichi Tanaka, Kanako Sonoda, Masato Asanuma

Advances in Parkinson's Disease 6 93 - 100 2017.8

Influence of nicotine on doxorubicin and cyclophosphamide combination treatment-induced spatial cognitive impairment and anxiety-like behavior in rats Reviewed

Yoshihisa Kitamura, Erika Kanemoto, Misaki Sugimoto, Ayumi Machida, Yuka Nakamura, Nanami Naito, Hirotaka Kanzaki, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

Naunyn-Schmiedeberg's Archives of Pharmacology 390 ( 4 ) 369 - 378 2017.4

Identification of transcription factors activated by methylmercury in mouse brain Reviewed

Min-Soek Kim, Tsutomu Takahashi, Jin-Yong Lee, Nobuhiko Miura, Masato Asanuma, Gi-Wook Hwang, Akira Naganuma

Fundamental Toxicological Sciences 4 ( 1 ) 37 - 39 2017

Therapeutic strategy of targeting astrocytes for neuroprotection in parkinson’s disease Reviewed

Ikuko Miyazaki, Masato Asanuma

Current Pharmaceutical Design 23 ( 33 ) 4936 - 4947 2017

Language：English Publishing type：Research paper (scientific journal) Publisher：Bentham Science Publishers B.V.

Parkinson’s disease (PD) is one of common neurodegenerative diseases, which shows motor symptoms including tremor, bradykinesia, rigidity and postural instability. It also involves non-motor symptoms such as cognitive impairment, mental manifestation, autonomic disorder and sensory disturbance. Although treatments to improve the motor disability in PD are being assessed at present, the main challenge remains that is the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find approaches that can inhibit the progression of dopaminergic neurodegeneration. Astrocytes are known to play an important role in the maintenance of the neuronal environment and exert neuroprotective effects. Additionally, astrocyte dysfunction increases the susceptibility of neurons to cytotoxicity. We have demonstrated neuroprotective approaches in parkinsonian models in various studies targeting astrocytes. In this article, we summarize the neuroprotective function of astrocytes in the brain, involvement of astrocyte dysfunction in neurodegeneration, and experimental approaches to dopaminergic neuroprotection. We review findings reported in several papers including our own studies. We also address target molecules and pivotal pathways in astrocytes for dopaminergic neuroprotection. The review discusses new promising therapeutic strategies to prevent dopaminergic neurodegeneration in PD.

DOI： 10.2174/1381612823666170710163731

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3-O-Methyldopa inhibits astrocyte-mediated dopaminergic neuroprotective effects of l-DOPA Reviewed

Masato Asanuma, Ikuko Miyazaki

BMC Neuroscience 17 ( 1 ) 52 2016.12

L-Theanine protects against excess dopamine-induced neurotoxicity in the presence of astrocytes Reviewed

Mika Takeshima, Ikuko Miyazaki, Shinki Murakami, Taizo Kita, Masato Asanuma

Journal of Clinical Biochemistry and Nutrition 59 ( 2 ) 93 - 99 2016.9

In vitro quantitative determination of the concentration of the polymerization agent methyl 2-benzoylbenzoate in intravenous injection solution and the cytotoxic effects of the chemical on normal human peripheral blood mononuclear cells Reviewed

Chiaki Tsuboi, Yoichi Kawasaki, Kei Yoshitome, Kenta Yagi, Taro Miura, Satoru Esumi, Ikuko Miyazaki, Masato Asanuma, Yoshihisa Kitamura, Toshiaki Sendo

Environmental Science and Pollution Research 23 ( 10 ) 10262 - 10269 2016.5

Neuroprotective effects of levetiracetam target xCT in astrocytes in parkinsonian mice Reviewed

Ikuko Miyazaki, Shinki Murakami, Nao Torigoe, Yoshihisa Kitamura, Masato Asanuma

Journal of Neurochemistry 136 ( 1 ) 194 - 204 2016.1

Anti-high mobility group box 1 antibody exerts neuroprotection in a rat model of Parkinson's disease Reviewed

Tatsuya Sasaki, Keyue Liu, Takashi Agari, Takao Yasuhara, Jun Morimoto, Mihoko Okazaki, Hayato Takeuchi, Atsuhiko Toyoshima, Susumu Sasada, Aiko Shinko, Akihiko Kondo, Masahiro Kameda, Ikuko Miyazaki, Masato Asanuma, Cesario V. Borlongan, Masahiro Nishibori, Isao Date

Experimental Neurology 275 220 - 231 2016.1

Changes in Metallothionein Isoform Expression in the Bones of Ovariectomized Rats Reviewed

Chiharu Sogawa, Mika Ikegame, Ikuko Miyazaki, Toshiaki Ara, Yasuhiro Imamura, Yuka Okusha, Kazumi Ohyama, Masato Asanuma, Norio Sogawa, Toshio Yamamoto, Ken-ichi Kozaki

Journal of Hard Tissue Biology 25 ( 1 ) 21 - 26 2016

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Papers - ASANUMA Masato