研究者業績

岩瀬 克郎

イワセ カツロウ  (Katsuro Iwase)

基本情報

所属
千葉大学 大学院医学研究院中核研究部門脳・神経治療学研究講座 講師
学位
博士(医学)(1998年3月 熊本大学)

研究者番号
80322030
J-GLOBAL ID
200901028745234054
researchmap会員ID
1000306438

外部リンク

経歴

 2

主要な論文

 31
  • Go Tomiyoshi, Rika Nakamura, Natsuko Shinmen, Yoichi Yoshida, Seiichiro Mine, Toshio Machida, Katsuro Iwase, Yasuo Iwadate, Takaki Hiwasa, Hideyuki Kuroda
    Frontiers in medicine 10 1128921-1128921 2023年  査読有り
    We previously identified growth arrest and DNA-damage-inducible gene 34 (GADD34) as a marker of ischemic stroke. In the present study, serum levels of anti-GADD34 antibodies were found to be significantly higher in patients with acute ischemic stroke or chronic kidney disease compared to healthy donors. We then examined the biological function of GADD34 by transfection into U2OS human osteosarcoma and U87 human glioblastoma cells. Knockdown of GADD34 by siRNA resulted in enhanced cell proliferation, which was reversed by co-knockdown of MDM2. Luciferase reporter assays revealed that the transactivation ability of p53 enhanced by genotoxic anticancer drugs such as camptothecin and etoposide was further potentiated by enforced expression of GADD34 but attenuated by co-transfection with p53 shRNA expression plasmids. Western blotting demonstrated increased p53 protein levels after treatment with camptothecin, which was also potentiated by GADD34 but suppressed by GADD34 siRNA, ATM siRNA, and ATM inhibitor wortmannin. GADD34 levels also increased in response to treatment with camptothecin or adriamycin, and this increase was attenuated by MDM2 siRNA. Immunoprecipitation with anti-GADD34 antibody followed by Western blotting with anti-MDM2 antibodies indicated ubiquitination of GADD34 is mediated by MDM2. Accordingly, GADD34 may function as a ubiquitination decoy to reduce p53 ubiquitination and increase p53 protein levels. Increased neuronal cell death due to activation of p53 by GADD34 may account for the elevated serum levels of anti-GADD34 antibodies observed in patients with acute ischemic stroke.
  • Shu-Yang Li, Yoichi Yoshida, Masaaki Kubota, Bo-Shi Zhang, Tomoo Matsutani, Masaaki Ito, Satoshi Yajima, Kimihiko Yoshida, Seiichiro Mine, Toshio Machida, Aiko Hayashi, Minoru Takemoto, Koutaro Yokote, Mikiko Ohno, Eiichiro Nishi, Kenichiro Kitamura, Ikuo Kamitsukasa, Hirotaka Takizawa, Mizuki Sata, Kazumasa Yamagishi, Hiroyasu Iso, Norie Sawada, Shoichiro Tsugane, Katsuro Iwase, Hideaki Shimada, Yasuo Iwadate, Takaki Hiwasa
    Frontiers in cardiovascular medicine 10 1042272-1042272 2023年  査読有り
    INTRODUCTION: Autoantibodies against inflammatory cytokines may be used for the prevention of atherosclerosis. Preclinical studies consider colony-stimulating factor 2 (CSF2) as an essential cytokine with a causal relationship to atherosclerosis and cancer. We examined the serum anti-CSF2 antibody levels in patients with atherosclerosis or solid cancer. METHODS: We measured the serum anti-CSF2 antibody levels via amplified luminescent proximity homogeneous assay-linked immunosorbent assay based on the recognition of recombinant glutathione S-transferase-fused CSF2 protein or a CSF2-derived peptide as the antigen. RESULTS: The serum anti-CSF2 antibody (s-CSF2-Ab) levels were significantly higher in patients with acute ischemic stroke (AIS), acute myocardial infarction (AMI), diabetes mellitus (DM), and chronic kidney disease (CKD) compared with healthy donors (HDs). In addition, the s-CSF2-Ab levels were associated with intima-media thickness and hypertension. The analyzes of samples obtained from a Japan Public Health Center-based prospective study suggested the utility of s-CSF2-Ab as a risk factor for AIS. Furthermore, the s-CSF2-Ab levels were higher in patients with esophageal, colorectal, gastric, and lung cancer than in HDs but not in those with mammary cancer. In addition, the s-CSF2-Ab levels were associated with unfavorable postoperative prognosis in colorectal cancer (CRC). In CRC, the s-CSF2-Ab levels were more closely associated with poor prognosis in patients with p53-Ab-negative CRC despite the lack of significant association of the anti-p53 antibody (p53-Ab) levels with the overall survival. CONCLUSION: S-CSF2-Ab was useful for the diagnosis of atherosclerosis-related AIS, AMI, DM, and CKD and could discriminate poor prognosis, especially in p53-Ab-negative CRC.
  • Shogo Moriya, Michiko Hanazono, Takeshi Fukuhara, Katsuro Iwase, Nobutaka Hattori, Masaki Takiguchi
    Cellular and molecular life sciences : CMLS 79(5) 234-234 2022年4月10日  査読有り
    Lewy body (LB), which mainly consists of abnormal α-synuclein (αS) aggregates, is a histological hallmark of Parkinson's disease (PD). αS aggregation and LB inclusions are induced by spreading αS fibrils to neurons; therefore, the formation and transmission of αS fibrils to neurons may play an essential role in initiating LB formation in neurons. αS expressed in neurons is released into the extracellular space and taken up by macrophages and microglia; therefore, we hypothesized that macrophages/microglia play a role in the formation and spread of αS fibrils. In this study, we aimed to investigate the involvement of macrophages/microglia in the formation and spread of αS fibrils using transgenic animals that express human αS in macrophages/microglia. Transgenic zebrafish expressing A53T mutated αS (αS_A53T) in macrophages/microglia revealed αS accumulation in neurons. Transcriptome analysis by RNA-seq of human αS and αS_A53T expressing zebrafish revealed that kinase genes and E3 ubiquitin protein ligase genes were significantly high, and neuronal activity and transport-related Gene Ontology terms were also isolated. Meanwhile, αS_A53T monomers were taken up by A-THP-1 cells; processed to larger molecules, which could be αS fibrils; and released from macrophage cells. Furthermore, the ubiquitin-proteasome system modulated αS fibrils in A-THP-1 cells. αS fibrils suggest being formed from monomers in macrophages and spread to neurons to induce αS aggregates. Therefore, macrophages may play an essential role in the formation of αS aggregates and the pathogenesis of PD.
  • Akiko Taira, Emiko Arita, Eriko Matsumoto, Ayano Oohira, Katsuro Iwase, Takaki Hiwasa, Koutaro Yokote, Shigenobu Shibata, Masaki Takiguchi
    Chronobiology international 36(5) 591-615 2019年5月  査読有り
    Gluconeogenesis is de novo glucose synthesis from substrates such as amino acids and is vital when glucose is lacking in the diurnal nutritional fluctuation. Accordingly, genes for hepatic gluconeogenic enzymes exhibit daily expression rhythms, whose detailed regulations under nutritional variations remain elusive. As a first step, we performed general systematic characterization of daily expression profiles of gluconeogenic enzyme genes for phosphoenolpyruvate carboxykinase (PEPCK), cytosolic form (Pck1), glucose-6-phosphatase (G6Pase), catalytic subunit (G6pc), and tyrosine aminotransferase (TAT) (Tat) in the mouse liver. On a standard diet fed ad libitum, mRNA levels of these genes showed robust daily rhythms with a peak or an elevation phase during the late sleep-fasting period in the diurnal feeding/fasting (wake/sleep) cycle. The rhythmicity was preserved in constant darkness, modulated with prolonged fasting, attenuated by Clock mutation, and entrained to varied photoperiods and time-restricted feedings. These results are concordant with the notion that gluconeogenic enzyme genes are under the control of the intrinsic circadian oscillator, which is entrained by the light/dark cycle, and which in turn entrains the feeding/fasting cycle and also drives systemic signaling pathways such as the hypothalamic-pituitary-adrenal axis. On the other hand, time-restricted feedings also showed that the ingestion schedule, when separated from the light/dark cycle, can serve as an independent entrainer to daily expression rhythms of gluconeogenic enzyme genes. Moreover, nutritional changes dramatically modified expression profiles of the genes. In addition to prolonged fasting, a high-fat diet and a high-carbohydrate (no-protein) diet caused modification of daily expression rhythms of the genes, with characteristic changes in profiles of glucoregulatory hormones such as corticosterone, glucagon, and insulin, as well as their modulators including ghrelin, leptin, resistin, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). Remarkably, high-protein (60% casein or soy-protein) diets activated the gluconeogenic enzyme genes atypically during the wake-feeding period, with paradoxical up-regulation of glucagon, which frequently formed correlation networks with other humoral factors. Based on these results, we propose that daily expression rhythms of gluconeogenic enzyme genes are under the control of systemic oscillator-driven and nutrient-responsive hormones.
  • Katsuro Iwase, Akinori Ishihara, Shuntaro Yoshimura, Yoshio Andoh, Masaki Kato, Naohiko Seki, Eriko Matsumoto, Takaki Hiwasa, Dominique Muller, Kohji Fukunaga, Masaki Takiguchi
    Journal of neurochemistry 128(2) 233-45 2014年1月  査読有り筆頭著者責任著者
    Cooperative gene regulation by different neurotransmitters likely underlies the long-term forms of associative learning and memory, but this mechanism largely remains to be elucidated. Following cDNA microarray analysis for genes regulated by Ca(2+) or cAMP, we found that the secretogranin II gene (Scg2) was cooperatively activated by glutamate and dopamine in primary cultured mouse hippocampal neurons. The Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM) and the mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor PD98059 prevented Scg2 activation by glutamate or dopamine; thus, the Ca(2+) /MEK pathway is predicted to include a convergence point(s) of glutamatergic and dopaminergic signaling. Unexpectedly, the protein kinase A inhibitor KT5720 enhanced Scg2 activation by dopamine. The protein-synthesis inhibitor cycloheximide also enhanced Scg2 activation, and the proteasome inhibitor ZLLLH diminished the KT5720-mediated augmentation of Scg2 activation. These results are concordant with the notion that dopaminergic input leads to accumulation of a KT5720-sensitive transcriptional repressor, which is short-lived because of rapid degradation by proteasomes. This repression pathway may effectively limit the time window permissive to Scg2 activation by in-phase glutamate and dopamine inputs via the Ca(2+) /MEK pathway. We propose that the regulatory system of Scg2 expression is equipped with machinery that is refined for the signal integration of in-phase synaptic inputs. We proposed hypothetical mechanism for the regulation of the secretogranin II gene as a signal integrator of glutamate and dopamine inputs. Glutamate or dopamine activates the Ca(2+) /MEK/ERK pathway, which thus contributes to the signal integration. Concurrently, activation of the PKA inhibitor KT5720-sensitive pathway by dopamine leads to accumulation of the repressor protein X that is otherwise susceptible to proteasome degradation. This repression system may determine the time window permissive to the cooperative activation by in-phase glutamate and dopamine inputs.
  • Osamu Miyauchi, Katsuro Iwase, Kanako Itoh, Masaki Kato, Naohiko Seki, Olivier Braissant, Claude Bachmann, Makio Shozu, Souei Sekiya, Hisao Osada, Masaki Takiguchi
    PloS one 8(11) e79236 2013年  査読有り筆頭著者
    Innate immune responses play a central role in neuroprotection and neurotoxicity during inflammatory processes that are triggered by pathogen-associated molecular pattern-exhibiting agents such as bacterial lipopolysaccharide (LPS) and that are modulated by inflammatory cytokines such as interferon γ (IFNγ). Recent findings describing the unexpected complexity of mammalian genomes and transcriptomes have stimulated further identification of novel transcripts involved in specific physiological and pathological processes, such as the neural innate immune response that alters the expression of many genes. We developed a system for efficient subtractive cloning that employs both sense and antisense cRNA drivers, and coupled it with in-house cDNA microarray analysis. This system enabled effective direct cloning of differentially expressed transcripts, from a small amount (0.5 µg) of total RNA. We applied this system to isolation of genes activated by LPS and IFNγ in primary-cultured cortical cells that were derived from newborn mice, to investigate the mechanisms involved in neuroprotection and neurotoxicity in maternal/perinatal infections that cause various brain injuries including periventricular leukomalacia. A number of genes involved in the immune and inflammatory response were identified, showing that neonatal neuronal/glial cells are highly responsive to LPS and IFNγ. Subsequent RNA blot analysis revealed that the identified genes were activated by LPS and IFNγ in a cooperative or distinctive manner, thereby supporting the notion that these bacterial and cellular inflammatory mediators can affect the brain through direct but complicated pathways. We also identified several novel clones of apparently non-coding RNAs that potentially harbor various regulatory functions. Characterization of the presently identified genes will give insights into mechanisms and interventions not only for perinatal infection-induced brain damage, but also for many other innate immunity-related brain disorders.
  • Eriko Matsumoto, Akinori Ishihara, Saki Tamai, Ayako Nemoto, Katsuro Iwase, Takaki Hiwasa, Shigenobu Shibata, Masaki Takiguchi
    The Journal of biological chemistry 285(43) 33028-33036 2010年10月22日  査読有り
    Sterol regulatory element-binding protein-1 (SREBP-1) plays a central role in transcriptional regulation of genes for hepatic lipid synthesis that utilizes diet-derived nutrients such as carbohydrates and amino acids, and expression of SREBP-1 exhibits daily rhythms with a peak in the nocturnal feeding period under standard housing conditions of mice. Here, we report that the Srebp-1 expression rhythm shows time cue-independent and Clock mutation-sensitive circadian nature, and is synchronized with varied photoperiods apparently through entrainment of locomotor activity and food intake. Fasting caused diminution of Srebp-1 expression, while diabetic db/db and ob/ob mice showed constantly high expression with loss of rhythmicity. Time-restricted feedings during mid-light and mid-dark periods exhibited differential effects, the latter causing more severe damping of the oscillation. Therefore, "when to eat in a day (the light/dark cycle)," rather than "whenever to eat in a day," is a critical determinant to shape the daily rhythm of Srebp-1 expression. We further found that a high-carbohydrate diet and a high-protein diet, as well as a high-fat diet, cause phase shifts of the oscillation peak into the light period, underlining the importance of "what to eat." Daily rhythms of SREBP-1 protein levels and Akt phosphorylation levels also exhibited nutrient-responsive changes. Taken together, these findings provide a model for mechanisms by which time of day and nutrients in feeding shape daily rhythms of the Srebp-1 expression and possibly a number of other physiological functions with interindividual and interdaily differences in human beings and wild animals subjected to day-by-day changes in dietary timing and nutrients.
  • Minoru Tomizawa, Yoshiro Toyama, Chizuru Ito, Kiyotaka Toshimori, Katsuro Iwase, Masaki Takiguchi, Hiromitsu Saisho, Osamu Yokosuka
    Cell and tissue research 333(1) 17-27 2008年7月  査読有り
    In order to enrich hepatocytes differentiated from embryonic stem cells, we developed a novel medium. Since only hepatocytes have the activity of ornithine transcarbamylase, phenylalanine hydroxylase, galactokinase, and glycerol kinase, we expected that hepatocytes would be enriched in a medium without arginine, tyrosine, glucose, and pyruvate, but supplemented with ornithine, phenylanaline, galactose, and glycerol (hepatocyte-selection medium, HSM). Embryoid bodies were transferred onto dishes coated with gelatin in HSM after 4 days of culture. At 18 days after embryoid body formation, a single type of polygonal cell survived with an enlarged intercellular space and micorvilli. These cells were positive for indocyanine green uptake and for mRNAs of albumin, transthyretin, and alpha-feto protein, but negative for mRNAs of tyrosine aminotransferase, alpha1-antitrypsin, glucose-6-phosphatase, and phosphoenol pyruvate carboxykinase. Since cells in HSM were positive for cytokeratin (CK)8 and CK18 (hepatocyte markers) and for CK19 (a marker of bile duct epithelial cells), we concluded that they were hepatoblasts. They showed weaker expression of CCAAT/enhancer-binding protein (C/EBP)alpha than fetal liver (18.5 days of gestation) and expression of C/EBPbeta at a similar level to that of fetal liver. These data support our conclusion that HSM allows the selection of hepatoblast-like cells.
  • Akinori Ishihara, Eriko Matsumoto, Kazumasa Horikawa, Takashi Kudo, Eiko Sakao, Ayako Nemoto, Katsuro Iwase, Hajime Sugiyama, Yutaka Tamura, Shigenobu Shibata, Masaki Takiguchi
    Journal of biological rhythms 22(4) 324-34 2007年8月  査読有り
    Spot14 is a putative transcriptional regulator for genes involved in fatty acid synthesis. The Spot14 gene is activated in response to lipogenic stimuli such as dietary carbohydrate and is also under circadian regulation. The authors investigated factors responsible for daily oscillation of Spot14 expression. If mice were kept under a 12-h light/12-h dark cycle with ad libitum feeding, Spot14 mRNA levels in the liver reached a peak at an early dark period when mice, as nocturnal animals, start feeding. Under fasting, while Spot14 mRNA levels were generally decreased, the rhythmicity was still maintained, suggesting contribution of both nutritional elements and circadian clock factors on robust rhythmicity of Spot14 expression. Effects of circadian clock factors were confirmed by the observations that the circadian rhythm of Spot14 expression was seen also under the constant darkness and that the rhythmicity was lost in Clock mutant mice. When mice were housed in short-photoperiod (6-h light/18-h dark) and long-photoperiod (18-h light/6-h dark) cycles, rhythms of Spot14 mRNA levels were phase advanced and phase delayed, respectively, being concordant with the notion that Spot14 expression is under the control of the light-entrainable oscillator. As for nutritional mediators, in the liver of db/db mice exhibiting hyperinsulinemia-accompanied hyperglycemia, Spot14 mRNA levels were constantly high without apparent rhythmicity, consistent with previous observations for strong activation of the Spot14 gene by glucose and insulin. Restricted feeding during the 4-h mid-light period caused a phase advance of the Spot14 expression rhythm. On the other hand, restricted feeding during the 4-h mid-dark period led to damping of the rhythmicity, apparently resulting from the separation of phases between effects of the light/dark cycle and feeding on Spot14 expression. Thus, the daily rhythm of Spot14 expression in the liver is under the control of the light-entrainable oscillator, food-entrainable oscillator, and food-derived nutrients, in a separate or cooperative manner.
  • Nobuyuki Kai, Katsuro Iwase, Kazuhide Imai, Eiko Nakahira, Miho Soma, Satoko Ohtsuka, Takeshi Yagi, Kazuto Kobayashi, Hisashi Koga, Masaki Takiguchi, Shigeki Yuasa
    Brain research 1073-1074 60-70 2006年2月16日  査読有り
    Fyn-tyrosine-kinase-deficient mice exhibit increased fearfulness and display enhanced excitability in the amygdala. To gain insight into the molecular changes associated with the increased excitability of the amygdala, we used a newly developed cDNA array system comprising mouse KIAA cDNA clones to identify novel genes differentially expressed in the amygdala of fyn(-/-) and fyn(+/-) mice following administration of N-methyl-D-aspartate (NMDA). Laser capture microdissection in combination with PCR-based cDNA amplification allowed us to analyze gene expression in each amygdalar subdivision. The statistical significance of the differential expressions was tested by one-way analysis of variance (ANOVA) by the false discovery rate controlling approach. Among the 805 mKIAA cDNA clones tested, only the expression level of mKIAA1577 (Zinc finger SWIM domain containing protein 6; gene name, Zswim6) showed statistically significant change in regard to the genotype and amygdalar subdivision. Namely, only the lowered expression of mKIAA1577 in the central nucleus of fyn(-/-) mice 1 h after NMDA administration (2.1-fold lower relative to fyn(+/-) mice) was statistically significant. In situ hybridization analysis confirmed the downregulation of the mRNA in the central nucleus of the fyn(-/-) mice 1 h after NMDA administration (3.2-fold lower relative to fyn(+/-) mice). The NMDA-induced change in gene expression was partially blocked by the NMDA antagonist D-AP-5. These results suggest that Fyn deficiency was responsible for the NMDA-induced downregulation of a specific gene in the amygdalar central nucleus.
  • Satoko Ohtsuka, Katsuro Iwase, Masaki Kato, Naohiko Seki, Atsuko Shimizu-Yabe, Osamu Miyauchi, Eiko Sakao, Masaki Kanazawa, Shigenori Yamamoto, Yoichi Kohno, Masaki Takiguchi
    Genomics 84(4) 715-29 2004年10月  査読有り
    We developed an integrated system suitable for comprehensive gene expression studies including construction and analysis of cDNA microarrays starting from a small amount of mRNA. We amplified total mRNA first as cDNA mixtures by polymerase chain reaction and then as strand-specific cRNA mixtures by in vitro transcription. These amplified cDNA and cRNA enabled determination of mRNA levels by hybridization analyses such as Southern, Northern, reverse-Northern macroarray, and cDNA microarray analyses, as well as construction of the cDNA library with a unidirectional cDNA insert. By using strand-specific cRNA derived from rat primary-cultured hepatocytes, we detected putative antisense transcripts for the metallothionein gene. cDNA microarray analysis for genes regulated by glucocorticoids and glucagon in the hepatocytes revealed that a number of genes involved in signal transduction and transcriptional regulation were up- or down-regulated. The present system is widely applicable to gene expression analysis with limited amounts of RNA samples.
  • Katsuro Iwase, Kei Miyanaka, Atsuko Shimizu, Akitoshi Nagasaki, Tomomi Gotoh, Masataka Mori, Masaki Takiguchi
    Journal of Biological Chemistry 275(16) 11929-11933 2000年4月  査読有り筆頭著者
    In the brain, three isoforms of nitric oxide (NO) synthase (NOS), namely neuronal NOS (nNOS, NOS1), inducible NOS (iNOS, NOS2), and endothelial NOS (eNOS, NOS3), have been implicated in biological roles such as neurotransmission, neurotoxicity, immune function, and blood vessel regulation, each isoform exhibiting in part overlapping roles. Previous studies showed that iNOS is induced in the brain by systemic treatment with lipopolysaccharide (LPS), a Gram-negative bacteria-derived stimulant of the innate immune system. Here we found that eNOS mRNA is induced in the rat brain by intraperitoneal injection of LPS of a smaller amount than that required for induction of iNOS mRNA. The induction of eNOS mRNA was followed by an increase in eNOS protein. Immunohistochemical analysis revealed that eNOS is located in astrocytes of both gray and white matters as well as in blood vessels. Induction of enos in response to a low dose of LPS, together with its localization in major components of the blood-brain barrier, suggests that brain eNOS is involved in early pathophysiologic response against systemic infection before iNOS is induced with progression of the infection.
  • Katsuro Iwase, Ken Ichi Iyama, Kiwamu Akagi, Shigetoshi Yano, Kohji Fukunaga, Eishichi Miyamoto, Masataka Mori, Masaki Takiguchi
    Molecular Brain Research 53(1-2) 1-12 1998年1月  査読有り筆頭著者
    Regional distribution of neurons expressing neuronal nitric oxide synthase mRNA in the rat brain was examined by non-radioisotopic in situ hybridization, using digoxigenin-labeled complementary RNA probes. Clustering of intensely positive neurons was observed in discrete areas including the main and accessory olfactory bulbs, the islands of Calleja, the amygdala, the paraventricular nucleus of the thalamus, several hypothalamic nuclei, the lateral geniculate nucleus, the magnocellular nucleus of the posterior commissure, the superior and inferior colliculi, the laterodorsal and pedunculopontine tegmental nuclei, the nucleus of the trapezoid body, the nucleus of the solitary tract and the cerebellum. Strongly-stained isolated neurons were scattered mainly in the cerebral cortex, the basal ganglia and the brain stem, especially the medulla reticular formation. In the hippocampus, an almost uniform distribution of moderately stained neurons was observed in the granular cell layer of the dentate gyrus and in the pyramidal cell layer of the Ammon's horn, while more intensely stained isolated neurons were scattered over the entire hippocampal region. These observations can serve as a good basis for studies on function and gene regulation of neuronal nitric oxide synthase.

MISC

 16
  • 岩瀬克郎, 吉村俊太朗, 安藤嘉男, 松本絵里子, 日和佐隆樹, 瀧口正樹
    日本分子生物学会年会講演要旨集 32nd(Vol.4) 2009年  
  • 吉村俊太朗, 岩瀬克郎, 松本絵里子, 日和佐隆樹, 瀧口正樹
    生化学 2008年  
  • 岩瀬克郎, 吉村俊太朗, 日和佐隆樹, 瀧口正樹
    生化学 2007年  
  • 岩瀬克郎, 石原顕紀, 加藤真樹, 福永浩司, MULLER Dominique, 関直彦, 瀧口正樹
    日本分子生物学会年会講演要旨集 28th 308 2005年11月25日  
  • 上原七生, 溝田淳, 安達恵美子, 山本修一, 石原顕紀, 岩瀬克郎, 大塚里子, 瀧口正樹, 加藤真樹, 二村好憲, 関直彦, 児玉大樹
    日本糖尿病眼学会誌 10 63-67 2005年8月28日  
  • 上原七生, 溝田淳, 安達恵美子, 石原顕紀, 岩瀬克郎, 大塚里子, 加藤真樹, 二村好憲, 児玉大樹
    日本眼科紀要 56(2) 85-89 2005年2月28日  
    目的:糖尿病網膜症における分子レベルでの病態生理を解明することを目的にマウス網膜自家製cDNAマイクロアレイを作製し,包括的遺伝子発現解析を行った.方法:マウス網膜由来のcDNAクローン2,880個を滴載したマイクロアレイを作製した.ストレプトゾトシン腹腔内注射後1,3ヵ月の糖尿病および対照マウス網膜由来の増幅cRNAを用いてアレイ解析を行った.結果:糖尿病網膜において発現亢進が認められた遺伝子の多くは,ミトコンドリアにおける酸化的リン酸化経路の遺伝子であった.結論:糖尿病網膜での酸化的リン酸化経路の遺伝子群の発現上昇は,糖尿病骨格筋において同遺伝子群の発現が抑制されているとの最近の知見と異なる結果であった.糖尿病網膜ではインスリン非依存的なグルコースの細胞内への過剰な流入に対する応答として,グルコース代謝が潜在的に活性化された状態にあると考えられた(著者抄録)
  • Nanami Uehara-Adachi, Atsushi Mizota, Emiko Adachi-Usami, Shuichi Yamamoto, Akinori Ishihara, Katsuro Iwase, Satoko Ohtsuka, Masaki Takiguchi, Masaki Kato, Yoshinori Nimura, Naohiko Seki, Hiroki Kodama
    Folia Ophthalmologica Japonica 56 85-89 2005年2月1日  査読有り
    Purpose: To clarify the molecular pathophysiology of diabetic retinopathy (DR), we performed comprehensive gene expression analysis of the mouse retina under diabetic conditions with an in-house cDNA microarray. Methods: We prepared a microarray harboring 2,880 cDNAs derived from a mouse retina. Amplified cRNAs of diabetic and age-matched control mouse retinas at 1 and 3 months after intraperitoneal injection of streptozotocin were subjected to array analysis. Results: Genes significantly up-regulated in the diabetic state were listed, and they included a number of genes for oxidative phosphorylation in mitochondoria. Conclusions: Our finding of up-regulation of genes for oxidative phosphorylation in the diabetic retina differs from recently reported findings of down-regulation of these genes in the skeletal muscle of diabetic mice. The diabetic retina seems to be in a potentially activated state for glucose metabolism, presumably because of an increase in insulin-independent glucose influx.
  • N Adachi, M Kato, N Seki, A Ishihara, K Iwase, H Kodama, A Mizota, E Adachi-Usami, M Takiguchi, S Yamamoto
    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE 45 U93-U93 2004年4月  
  • 安達七生, 加藤真樹, 二村好憲, 関直彦, 石原顕紀, 岩瀬克郎, 児玉大樹, 溝田淳, 安達恵美子
    日本眼科学会雑誌 108 179 2004年3月15日  
  • 岩瀬 克郎, 大塚 里子, 滝口 正樹, 志水 加代
    千葉大学共同研究推進センター共同研究成果報告書 3 80-82 2002年9月20日  
  • 大塚里子, 岩瀬克郎, 加藤真樹, 関直彦, 宮内修, 坂尾詠子, 河野陽一, 滝口正樹
    生化学 73(8) 705 2001年8月25日  
  • 黒岩波子, 加藤真樹, 関直彦, 森居真史, 矢部(清水)淳子, 岩瀬克郎, 滝口正樹, 日和佐隆樹
    生化学 73(8) 716 2001年8月25日  
  • 森居真史, 加藤真樹, 関直彦, 黒岩波子, 岩瀬克郎, 江原正明, 税所宏光, 滝口正樹, 日和佐隆樹
    生化学 73(8) 719 2001年8月25日  
  • 親泊 政一, 木村 竜也, 岩瀬 克郎, 荒木 栄一, 七里 元亮, 森 正敬, 滝口 正樹
    日本分子生物学会年会プログラム・講演要旨集 21 427-427 1998年12月1日  
  • 岩瀬克郎, HEFFTStefan, 福永浩司, 宮本英七, 森正敬, MULLERDominique, 滝口正樹
    日本分子生物学会年会プログラム・講演要旨集 19 362-362 1996年8月1日  
  • Fumihiko Matsuno, Shoaib Chowdhury, Tomomi Gotoh, Katsuro Iwase, Hiromitsu Matsuzaki, Kiyoshi Takatsuki, Masataka Mori, Masaki Takiguchi
    Journal of Biochemistry 119 524-532 1996年1月1日  
    The synthetic glucocorticoid, dexamethasone, and glucagon cooperatively elevated the level of mRNA for the transcription factor CCAAT/enhancer binding protein β(C/EBPβ) in primary-cultured rat hepatocytes. In response to dexamethasone and/or glucagon, C/ EBPβ mRNA started to increase as early as at 30 min, reached a maximum within 2 h, and then gradually decreased. The administration of cycloheximide, a protein synthesis inhibitor, led rather to an increase in C/EBPβ mRNA, which suggested that a labile negative protein factor(s) is involved in regulation of the C/EBPβ mRNA level. Cycloheximide further augmented the increases in C/EBPβ mRNA by dexamethasone and/or glucagon. Therefore, C/EBPβ mRNA accumulation in response to these hormones is apparently independent of ongoing protein synthesis. The elevation of the C/EBPβ mRNA level by these hormones was accounted for by increases in the rate of transcription of the C/EBPβ gene, as deduced on nuclear run-on analysis. Gel mobility shift analysis revealed that the DNA-binding activity of C/EBPβ was increased cooperatively by dexamethasone and glucagon. These results suggest that the C/EBPβ gene is primarily induced by glucocorticoids and/or glucagon and that the accumulated C/EBPβ protein is then involved in secondary activation of target genes in response to these hormones in the liver.

共同研究・競争的資金等の研究課題

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