研究者詳細 - 宮﨑　育子

論文 - 宮﨑　育子

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Common anti-inflammatory drugs are potentially therapeutic for Parkinson's disease? 査読

Masato Asanuma, Ikuko Miyazaki

EXPERIMENTAL NEUROLOGY 206 ( 2 ) 172 - 178 2007年8月

Suppression of p53-activated gene, PAG608, attenuates methamphetamine-induced neurotoxicity 査読

Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Francisco J. Diaz-Corrales, Masako Shimizu, Ko Miyoshi, Norio Ogawa

NEUROSCIENCE LETTERS 414 ( 3 ) 263 - 267 2007年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ELSEVIER IRELAND LTD

The p53-activated gene 608 (PAG608) is a proapoptotic gene activated and regulated by p53 expression in oxidative stress-induced apoptosis of neuronal cells. In this study, we determined the role of PAG608 in methamphetamine-induced neurotoxicity. Treatment of mouse dopaminergic CATH.a cells with 2 mM methamphetamine increased PAG608 expression at 3 h followed by increase in phosphorylated p53 expression. Transient transfection of PAG608 antisense cDNA or RNA interference using PAG608 small interfering RNA significantly attenuated the dose-dependent decrease in cell viability of CATH.a cells by methamphetamine (1-4 mM) exposure. In monoaminergic neuronal B65 cells, which contain serotonin rather than dopamine, methamphetamine-induced cell death was also significantly but partially protected by transient transfection of PAG608 antisense cDNA. Furthermore, cell death of PC 12 cells produced by methamphetamine (1-5 mM) was almost completely prevented by stable expression of PAG608 antisense cDNA, compared with significant reduction of cell viability in control PC12 cells. Our results showed that suppression of PAG608 using transient and stable transfection with PAG608 anti sense cDNA or small interfering RNA attenuates methamphetamine-induced death of various monoaminergic neuronal cells, suggesting that methamphetamine neurotoxicity in monoaminergic cells is related, at least in part, to induction of PAG608 expression. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.neulet.2006.12.036

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食品容器および食器より溶出する化学物質のドパミン神経障害性に関する研究－ビスフェノールＡの培養ドパミン神経系への作用－

喜多大三, 竹島美香, 田中弓子, 宮崎育子, 浅沼幹人

九州栄養福祉大学研究紀要 4 ( 4 ) 89 - 97 2007年

Involvement of STAT3 in bladder smooth muscle hypertrophy following bladder outlet obstruction

Osamu Fujita, Masato Asanuma, Teruhiko Yokoyama, Ikuko Miyazaki, Norio Ogawa, Hiromi Kumon

ACTA MEDICA OKAYAMA 60 ( 6 ) 299 - 309 2006年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：OKAYAMA UNIV MED SCHOOL

We examined the involvement of the signal transducer and activator of transcription 3 (STAT3) in bladder outlet obstruction (BOO)-induced bladder smooth muscle hypertrophy using a rat in vivo and in vitro study. BOO induced increases in bladder weight and bladder smooth muscle thickness I week after the operation. By using antibody microarrays, 64 of 389 proteins blotted on the array met our selection criteria of an INR value between >= 2.0 and <= 0.5. This result revealed up-regulation of transcription factors, cell cycle regulatory proteins, apoptosis-associated proteins and so on. On the other hand, down-regulation (INR value <= 0.5) of proteins was not found. In a profiling study, we found an increase in the expression of STAT3. A significant increase in nuclear phosphorylated STAT3 expression was confirmed in bladder smooth muscle tissue by immunohistochemistry and Western blot analysis. Cyclical stretch-relaxation (I Hz) at 120% elongation significantly increased the expression of STAT3 and of alpha-smooth muscle actin in primary cultured bladder smooth muscle cells. Furthermore, the blockade of STAT3 expression by the transfection of STAT3 small interfering RNA (siRNA) significantly prevented the stretch-induced increase in alpha-smooth muscle actin expression. These results suggest that STAT3 has an important role in the induction of bladder smooth muscle hypertrophy.

DOI： 10.18926/AMO/30724

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Characterization of pericentrin isoforms in vivo 査読

Ko Miyoshi, Masato Asanuma, Ikuko Miyazaki, Shinsuke Matsuzaki, Masaya Tohyama, Norio Ogawa

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 351 ( 3 ) 745 - 749 2006年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：ACADEMIC PRESS INC ELSEVIER SCIENCE

Pericentrin was first identified as a mouse centrosomal protein and is now referred to as pericentrin A. A larger homologous protein in humans with a C-terminal calmodulin-binding domain was later identified as pericentrin B. Pericentrin has been shown to be one of the key components in ciliogenesis.. but in vivo pericentrin products have remained ambiguous. Here we characterized pericentrin isoforms in mice. Two pericentrin transcripts of 9.5 and 6.9 kb were recognized on the mouse tissue Northern blots, while a cRNA probe for a 5'-terminal sequence shared by pericentrin A and B failed to hybridize to the 6.9-kb message. Two pericentrin cDNAs were identified, which encoded pericentrin B and a novel isoform, pericentrin S, sharing with pericentrin B a C-terminal calmodulin-binding motif. Three pericentrin proteins of 360, 255, and 250 kDa revealed by immunoprecipitation analysis were thought to correspond to pericentrin B, pericentrin S, and an unknown N-terminal product. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2006.10.101

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Nonsteroidal anti-inflammatory drugs in Parkinson’s disease: possible involvement of quinone formation 査読

Masato Asanuma, Ikuko Miyazaki

Expert Review of Neurotherapeutics 6 ( 9 ) 1313 - 1325 2006年9月

Embryonic expression of pericentrin suggests universal roles in ciliogenesis 査読

Ko Miyoshi, Kazunari Onishi, Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Norio Ogawa

DEVELOPMENT GENES AND EVOLUTION 216 ( 9 ) 537 - 542 2006年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：SPRINGER

Pericentrin (Pcnt) is a giant coiled-coil protein known to mediate microtubule organization. It has been recently reported that mitosis-specific centrosomal anchoring of gamma tubulin complexes by Pcnt acts to control mitotic spindle organization, though little is known about the in vivo expression of Pcnt. In this study, we investigated Pcnt expression in mouse embryos. In situ hybridization analysis revealed preferential expression of Pcnt in quiescent G(0) phase cells throughout the embryo with an unexpectedly low expression level in proliferating cells, suggesting that Pcnt might not play an important role in mitotic proliferation. Immunofluorescence analysis confirmed preferential expression of the Pcnt protein in G(0) phase cells. Moreover, Pcnt was shown to be localized to the base of primary cilia in multiple embryonic tissues, in agreement with a recent study demonstrating the involvement of Pcnt in primary cilia formation using cultured mammalian cells.

DOI： 10.1007/s00427-006-0065-8

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Centrosome overduplication induced by rotenone treatment affects the cellular distribution of p53 tumor suppressor protein in the neuroblastoma B65 cell line 査読

Francisco J. Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

PSYCHIATRY AND CLINICAL NEUROSCIENCES 60 S18 - S26 2006年4月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：BLACKWELL PUBLISHING

Recently, the formation of inclusion bodies in several neurodegenerative diseases, including Parkinson's disease, has been associated with the aggregation of unfolded proteins recruited in the centrosome. We have reported previously that rotenone, an insecticide that is used to produce experimental models of Parkinsonism, induced the aggregation of the alpha-synuclein protein in the centrosome, and it notably affected the structure and function of this organelle in primary cultures of mesencephalic neurons and astrocytes. However, it is still obscure the mechanisms through which the disorganization and centrosomal dysfunction could induce cell death. In this study the rat neuroblastoma B65 cell line was chronically exposed to rotenone, and then the distribution of the centrosomal protein gamma-tubulin was studied by immunocytochemistry and Western blot analyses. Finally, the configuration of mitotic spindles and distribution of the p53 protein was observed in the control and rotenone-treated groups. Rotenone treatment increased the number of cells having centrosome overduplication and multipolar mitotic spindles. In contrast, rotenone induced redistribution of the p53 protein, which was colocalized with the gamma-tubulin protein in the perinuclear region of cells having overduplicated centrosomes. In addition, the p53 positive signal was markedly intense in cells containing aberrant chromosome segregation and micronuclei. Our results suggest that centrosome overduplication may play an important role in the redistribution of the p53 protein in rotenone-treated cells, and this could represent an alternative mechanism of rotenone to induce apoptosis in neuronal cells.

DOI： 10.1111/j.1440-1819.2006.01526.x

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L-DOPA treatment from the viewpoint of neuroprotection - Possible mechanism of specific and progressive dopaminergic neuronal death in Parkinson's disease 査読

Norio Ogawa, Masato Asanuma, Ikuko Miyazaki, FJ Diaz-Corrales, Ko Miyoshi

JOURNAL OF NEUROLOGY 252 23 - 31 2005年10月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：DR DIETRICH STEINKOPFF VERLAG

With regard to the mechanism of selective dopaminergic neuronal death, experimental results of studies on the neurotoxicity of MPTP and rotenone indicate that degeneration of dopamine neurons is closely related to mitochondrial dysfunction, inflammatory process and oxidative stress, particularly with regard to the generation of quinones as dopamine neuron-specific oxidative stress. Thus, it is now clear that the presence of high levels of discompartmentalized free dopamine in sdopaminergic neurons may explain the specific vulnerability of dopaminergic neurons through the generation of highly toxic quinones.

DOI： 10.1007/s00415-005-4006-7

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Prednisolone Inhibits Proliferation of Cultured Pulmonary Artery Smooth Muscle Cells of Patients With Idiopathic Pulmonary Arterial Hypertension 査読国際誌

Aiko Ogawa, Kazufumi Nakamura, Hiromi Matsubara, Hideki Fujio, Tetsuya Ikeda, Kaoru Kobayashi, Ikuko Miyazaki, Masato Asanuma, Katsumasa Miyaji, Daiji Miura, Kengo Fukushima Kusano, Hiroshi Date, Tohru Ohe

Circulation 112 ( 12 ) 1806 - 1812 2005年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Ovid Technologies (Wolters Kluwer Health)

<bold>
<italic>Background—</italic>
</bold>
Idiopathic pulmonary arterial hypertension (IPAH) is associated with proliferation of smooth muscle cells (SMCs) in small pulmonary arteries. There is no therapy that specifically inhibits SMC proliferation. Recent studies reported that prednisolone (PSL) inhibits the postangioplasty proliferation of SMCs in atherosclerotic arteries. In this study, we tested the hypothesis that PSL has antiproliferative effects on pulmonary artery SMCs of patients with IPAH.

<bold>
<italic>Methods and Results—</italic>
</bold>
Pulmonary artery SMCs were harvested from the pulmonary arteries of 6 patients with IPAH who underwent lung transplantation. Control SMCs were obtained from 5 patients with bronchogenic carcinoma who underwent lung lobectomy. After incubation in the presence of platelet-derived growth factor (PDGF), PSL was added at different concentrations and cell proliferation was assessed by
³
H-thymidine incorporation. PSL (2×10
⁻⁴
and 2×10
⁻³
mol/L) significantly inhibited PDGF-stimulated proliferation (
<italic>P</italic>
<0.05) of SMCs from patients with IPAH but did not affect cell viability of SMCs, as confirmed by trypan blue staining. In cell cycle analysis using a microscope-based multiparameter laser scanning cytometer, PSL inhibited the progression of SMCs from G
₀
/G
₁
to the S phase. This inhibition was associated with increased p27 expression level. PSL (2×10
⁻⁴
mol/L) also inhibited PDGF-induced SMC migration.

<bold>
<italic>Conclusions—</italic>
</bold>
Our results indicate that PSL has an antiproliferative effect on cultured SMCs of pulmonary arteries from patients with IPAH and suggest that PSL may be potentially useful therapeutically in patients with IPAH.

DOI： 10.1161/circulationaha.105.536169

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Pramipexole has ameliorating effects on levodopa-induced abnormal dopamine turnover in parkinsonian striatum and quenching effects on dopamine-semiquinone generatedin vitro 査読

Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Masako Shimizu, Ken-ichi Tanaka, Norio Ogawa

Neurological Research 27 ( 5 ) 533 - 539 2005年7月

Rotenone induces aggregation of γ-tubulin protein and subsequent disorganization of the centrosome: Relevance to formation of inclusion bodies and neurodegeneration 査読

Francisco J. Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

Neuroscience 133 ( 1 ) 117 - 135 2005年1月

薬物依存・毒性発現にかかわる分子の分子生物学的検索法─網羅的プロファイリングを中心に.

浅沼幹人, 宮崎育子

日本薬理学雑誌 126, 30-34 ( 1 ) 30 - 34 2005年

記述言語：日本語出版者・発行元：公益社団法人日本薬理学会

従来，ある事象に関与すると考えられる分子の同定は，既知の関与分子と連関のあると報告された分子の発現の増減を一つ一つ確認していく，あるいは既知の分子と結合するタンパクをFar-Western法，two-hybrid法などで見つけていくという手法が用いられてきた．しかし，これではある事象に関与する既知の分子機構の枠を越えた新たな分子機構を発見したり，新たな観点に基づく分子仮説を提唱できるような発見をすることは難しかった．これに対して，10-20年前から，ある事象で発現が増減しているmRNAをスクリーニングする手法として，differential display法とそれに続くライブラリースクリーニング，RACE法などが広く用いられ，キット化された．さらに，近年1,000-10,000ものcDNA断片をブロットしたナイロン・グラス・プラスチックcDNAアレイが市販あるいはオーダーメードされるようになり，様々な生物学的・病理学的事象で発現が変化している遺伝子の網羅的検索が可能になった．近年のポストゲノムの潮流と遺伝子とタンパクの発現の乖離から，二次元電気泳動などによる発現タンパクのスクリーニング，さらに抗体がブロットされた抗体アレイを用いてのタンパク発現の網羅的検索も可能になってきている．しかし，これらの網羅的検索法はそれぞれ長所および短所，限界を有しており，目的に応じて使い分ける必要がある．本稿では，主に覚醒剤の急性毒性発現にかかわる遺伝子・分子の分子生物学的網羅的検索法の自検例を交えて，それらの長所・短所について概説する．<br>

DOI： 10.1254/fpj.126.30

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Quinone formation as dopaminergic neuron-specific oxidative stress in the pathogenesis of sporadic Parkinson's disease and neurotoxin-induced parkinsonism. 査読

Asanuma Masato, Miyazaki Ikuko, Diaz-Corrales Francisco J, Ogawa Norio

Acta Medica Okayama 58 ( 5 ) 221 - 233 2004年10月

記述言語：英語出版者・発行元：Okayama University Medical School

<p>Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by dopaminergic neuron-specific degeneration in the substantia nigra. A number of gene mutations and deletions have been reported to play a role in the pathogenesis of familial PD. Moreover, a number of pathological and pharmacological studies on sporadic PD and dopaminergic neurotoxin-induced parkinsonism have hypothesized that mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system all play important roles in the pathogenesis and progress of PD. However, these hypotheses do not yet fully explain the mechanisms of dopaminergic neuron-specific cell loss in PD. Recently, the neurotoxicity of dopamine quinone formation by auto-oxidation of dopamine has been shown to cause specific cell death of dopaminergic neurons in the pathogenesis of sporadic PD and dopaminergic neurotoxin-induced parkinsonism. Furthermore, this quinone formation is closely linked to other representative hypotheses in the pathogenesis of PD. In this article, we mainly review recent studies on the neurotoxicity of quinone formation as a dopaminergic neuron-specific oxidative stress and its role in the etiology of PD, in addition to several neuroprotective approaches against dopamine quinone-induced toxicity.</p>

DOI： 10.18926/AMO/32105

Specific Gene Expression and Possible Involvement of Inflammation in Methamphetamine-Induced Neurotoxicity 査読

Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Takeshi Tsuji, Norio Ogawa

Annals of the New York Academy of Sciences 1025 ( 1 ) 69 - 75 2004年10月