Updated on 2023/12/26

写真a

 
Sato Ikumi
 
Organization
Faculty of Health Sciences Assistant Professor
Position
Assistant Professor
Homepage
https://okadaihirohatalab.jimdofree.com/
External link

Degree

  • Doctor（Health Sciences） ( 2023.3   Okayama University )

  • Master (Health Sciences) ( 2021.3   Okayama University )

  • Bachelor (Health Sciences) ( 2019.3   Okayama University )

Research Interests

  • Exosome

  • atherosclerosis

  • 細胞外小胞

  • NASH

Research Areas

  • Others / Others  / 循環器病学

  • Life Science / Nutrition science and health science

  • Others / Others  / 病態検査学

Education

  • Okayama University   大学院保健学研究科   検査技術科学分野

    2021.4 - 2023.3

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    Notes： 博士後期課程

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  • Okayama University   大学院保健学研究科   検査技術科学分野

    2019.4 - 2021.3

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    Notes： 博士前期課程

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  • Okayama University   医学部   保健学科 検査技術科学分野

    2015.4 - 2019.3

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Research History

  • Okayama University   学術研究院保健学域 検査技術科学分野   Assistant Professor

    2022.10

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  • Okayama University   医学部保健学科

    2021.10 - 2022.3

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Professional Memberships

  • 日本細胞外小胞学会

    2022.10

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  • 高血圧関連疾患モデル学会

    2019.11

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  • 日本臨床衛生検査技師会

    2019.5

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  • 日本超音波検査学会

    2019.4

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  • 日本動脈硬化学会

    2019.1

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  • 日本食品安全協会

    2018.9

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Papers

  • Selective autophagy associated with iron overload aggravates non-alcoholic steatohepatitis via ferroptosis. Reviewed International journal

    Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Toshiaki Ohara, Kazuya Kitamori, Ikumi Sato, Satoshi Hirohata, Moe Fujii, Shusei Yamamoto, Shang Ran, Shogo Watanabe

    Experimental biology and medicine (Maywood, N.J.)   15353702231191197 - 15353702231191197   2023.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    Non-alcoholic steatohepatitis (NASH) is a progressive form of non-alcoholic fatty liver disease (NAFLD) that causes cirrhosis and hepatocellular carcinoma. Iron is an essential trace element in the body; however, excess iron can cause tissue damage and dysfunction. Iron overload is often observed in patients with NASH, and the amount of iron accumulated in the liver positively correlates with the histological severity of NASH. Ferroptosis, a novel form of iron-dependent cell death, is caused by the accumulation of lipid peroxidation and oxidative stress and is related to NASH. In addition, ferroptosis is closely related to autophagy, an intracellular self-degradation process. Although autophagy has many beneficial effects, it may also be harmful to the organism, for example, inducing ferroptosis. It is unclear whether iron overload aggravates NASH via autophagy. The aim of this research is to determine the mechanism by which iron overload induces ferroptosis via autophagy and aggravates NASH. Stroke-prone spontaneously hypertensive rats (SHRSP5/Dmcr) were divided into two groups and fed a high-fat and high-cholesterol (HFC) diet for eight weeks. Iron dextran was administered to the Fe group in addition to the HFC diet. Blood analysis, histological staining, calcineurin activity assay, quantitative reverse transcription polymerase chain reaction (RT-PCR), immunofluorescence staining, and electron microscopy were performed. The results showed that iron overload promoted autophagy via nuclear translocation of transcription factor EB (TFEB) and induced ferritinophagy, which is the autophagic degradation of ferritin. In addition, the HFC diet induced lipophagy, the autophagic degradation of lipid droplets. The Fe group also exhibited promoted ferroptosis and aggravated hepatic inflammation and fibrosis. In conclusion, iron overload accelerates ferritinophagy and lipophagy, aggravating NASH pathology via ferroptosis. These findings indicate the therapeutic potential of inhibiting autophagy and ferroptosis for treating NASH.

    DOI： 10.1177/15353702231191197

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  • Antioxidant action of xanthine oxidase inhibitor febuxostat protects the liver and blood vasculature in SHRSP5/Dmcr rats. Reviewed International journal

    Mai Kakimoto, Moe Fujii, Ikumi Sato, Koki Honma, Hinako Nakayama, Sora Kirihara, Taketo Fukuoka, Shang Ran, Satoshi Hirohata, Kazuya Kitamori, Shusei Yamamoto, Shogo Watanabe

    Journal of applied biomedicine   21 ( 2 )   80 - 90   2023.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Xanthine oxidase (XO) generates reactive oxygen species during uric acid production. Therefore, XO inhibitors, which suppress oxidative stress, may effectively treat non-alcoholic steatohepatitis (NASH) and atherosclerosis via uric acid reduction. In this study, we examined the antioxidant effect of the XO inhibitor febuxostat on NASH and atherosclerosis in stroke-prone spontaneously hypertensive 5 (SHRSP5/Dmcr) rats. METHODS: SHRSP5/Dmcr rats were divided into three groups: SHRSP5/Dmcr + high-fat and high-cholesterol (HFC) diet [control group, n = 5], SHRSP5/Dmcr + HFC diet + 10% fructose (40 ml/day) [fructose group, n = 5], and SHRSP5/Dmcr + HFC diet + 10% fructose (40 ml/day) + febuxostat (1.0 mg/kg/day) [febuxostat group, n = 5]. Glucose and insulin resistance, blood biochemistry, histopathological staining, endothelial function, and oxidative stress markers were evaluated. RESULTS: Febuxostat reduced the plasma uric acid levels. Oxidative stress-related genes were downregulated, whereas antioxidant factor-related genes were upregulated in the febuxostat group compared with those in the fructose group. Febuxostat also ameliorated inflammation, fibrosis, and lipid accumulation in the liver. Mesenteric lipid deposition decreased in the arteries, and aortic endothelial function improved in the febuxostat group. CONCLUSIONS: Overall, the XO inhibitor febuxostat exerted protective effects against NASH and atherosclerosis in SHRSP5/Dmcr rats.

    DOI： 10.32725/jab.2023.009

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  • Uric acid elevation by fructose overload exacerbates NASH and atherosclerosis via oxidative stress Reviewed

    Moe Fujii, Mai Kakimoto, Ikumi Sato, Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Satoshi Hirohata, Kazuya Kitamori, Shang Ran, Shusei Yamamoto, Shogo Watanabe

    Current nutrition and food science   20 ( 2 )   250 - 261   2023.6

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  • Therapeutic effect of ouabagenin, a novel liver X receptor agonist, on atherosclerosis in nonalcoholic steatohepatitis in SHRSP5/Dmcr rat model Reviewed

    Shusei Yamamoto, Ikumi Sato, Moe Fujii, Mai Kakimoto, Koki Honma, Sora Kirihara, Hinako Nakayama, Taketo Fukuoka, Satoru Tamura, Minoru Ueda, Satoshi Hirohata, Shogo Watanabe

    Canadian Journal of Physiology and Pharmacology   2023.5

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    Publishing type：Research paper (scientific journal)   Publisher：Canadian Science Publishing  

    The liver X receptor (LXR) can enhance cholesterol transporters, which could remove excess cholesterol from foam cells in atheromas. LXR has two subtypes: LXRα, which aggravates hepatic lipid accumulation, and LXRβ, which does not. In 2018, ouabagenin (OBG) was reported as a potential LXRβ-specific agonist. We aimed to examine whether OBG specifically affects LXRβ in nonalcoholic steatohepatitis (NASH); it did not aggravate hepatic steatosis and can suppress the development of atherosclerosis. SHRSP5/Dmcr rats fed a high-fat and high-cholesterol diet were divided into four groups as follows: (I) L-NAME group, (II) L-NAME/OBG group, (III) OBG (－) group, and (IV) OBG (+) group. All groups’ rats were intraperitoneally administered L-NAME. The L-NAME/OBG groups’ rats were intraperitoneally administered OBG and L-NAME simultaneously. After L-NAME administration, the OBG (+) groups’ rats were administered OBG, while the OBG (－) groups’ rats were not. Although all rats developed NASH, OBG did not exacerbate steatosis (L-NAME/OBG and OBG (+) groups). In addition, endothelial cells were protected in the L-NAME/OBG group and foam cells in the atheroma were reduced in the OBG (+) group. OBG is an LXRβ-specific agonist and has a potential therapeutic effect on atherosclerosis without developing lipid accumulation in the liver.

    DOI： 10.1139/cjpp-2022-0532

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  • SHRSP5/Dmcr rats fed a high-fat and high-cholesterol diet develop disease-induced sarcopenia as nonalcoholic steatohepatitis progresses. Reviewed International journal

    Shusei Yamamoto, Koki Honma, Moe Fujii, Mai Kakimoto, Sora Kirihara, Hinako Nakayama, Kazuya Kitamori, Ikumi Sato, Satoshi Hirohata, Shogo Watanabe

    Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft   152104 - 152104   2023.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Secondary sarcopenia develops as a result of a bedridden state and illnesses, such as cachexia, liver disease, and diabetes. However, there is a lack of animal models to investigate the underlying mechanisms and potential treatments for secondary sarcopenia. Recently, secondary sarcopenia has been associated with the prognosis of nonalcoholic steatohepatitis. This study aimed to investigate whether stroke-prone spontaneously hypertensive rat 5 (SHRSP5/Dmcr) which developed severe nonalcoholic steatohepatitis by a high-fat and high-cholesterol (HFC; containing 2% cholic acid) diet is a useful model of secondary sarcopenia. METHODS: SHRSP5/Dmcr rats were divided into 6 groups fed with a Stroke-Prone (SP: normal chow) or HFC diets for different periods (4, 12, and 20 weeks), and WKY/Izm rats were divided into 2 groups fed an SP or HFC diet. Body weight, food intake, and muscle force were measured weekly for all rats. After the end of the diet period, skeletal muscle strength evoked by electrical stimulation was recorded, blood was collected, and organ weight was measured. The sera were used for biochemical analysis and the organs were used for histopathological analysis. RESULTS: SHRSP5/Dmcr rats fed an HFC diet developed nonalcoholic steatohepatitis, and their skeletal muscles, especially fast muscles, showed atrophy, indicating that muscle atrophy is aggravated by the progression of nonalcoholic steatohepatitis. In contrast, WKY/Izm rats fed an HFC diet did not exhibit sarcopenia. CONCLUSIONS: This study suggests that SHRSP5/Dmcr rats could be a useful novel model for investigate the mechanism of secondary sarcopenia disorder associated with nonalcoholic steatohepatitis.

    DOI： 10.1016/j.aanat.2023.152104

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  • Increased Glycine-conjugated and Unconjugated Bile Acid Levels Associated with Aggravation of Nonalcoholic Steatohepatitis and Cardiovascular Disease in SHRSP5/Dmcr Rat. Reviewed

    Shusei Yamamoto, Ikumi Sato, Moe Fujii, Mai Kakimoto, Koki Honma, Natsumi Akiyama, Miku Sakai, Natsuki Fukuhama, Shota Kumazaki, Satoshi Hirohata, Kazuya Kitamori, Yukio Yamori, Shogo Watanabe

    Acta medica Okayama   77 ( 1 )   29 - 36   2023.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    The SHRSP5/Dmcr is a useful animal model for the development of nonalcoholic steatohepatitis (NASH) pathology when fed a high-fat, high-cholesterol diet, and further drug interventions can lead to concomitant cardiovascular disease. While SHRSP5/Dmcr rats have been used for basic research related to NASH, details of their bile acid metabolism in this condition are unknown. In this study, we aimed to clarify the changes in the serum bile acid (BA) fractions associated with NASH and found that glycine-conjugated and unconjugated bile acid increased with worsening NASH and cardiovascular disease while taurine-conjugated BA relatively decreased.

    DOI： 10.18926/AMO/64358

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  • Suppression of nitric oxide synthase aggravates non-alcoholic steatohepatitis and atherosclerosis in SHRSP5/Dmcr rat via acceleration of abnormal lipid metabolism. Reviewed International journal

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Shota Kumazaki, Mami Matsui, Hinako Nakayama, Sora Kirihara, Shang Ran, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

    Pharmacological reports : PR   74 ( 4 )   669 - 683   2022.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    BACKGROUND: Non-alcoholic steatohepatitis (NASH) is a progressive subtype of non-alcoholic fatty liver disease (NAFLD) that is closely related to cardiovascular disease (CVD). Nitric oxide (NO) plays a critical role in the control of various biological processes. Dysfunction of the NO signaling pathway is associated with various diseases such as atherosclerosis, vascular inflammatory disease, and diabetes. Recently, it has been reported that NO is related to lipid and cholesterol metabolism. Chronic NO synthase (NOS) inhibition accelerates NAFLD by increasing hepatic lipid deposition. However, the detailed relationship between NO and abnormal lipid and cholesterol metabolism in NAFLD/NASH has not been completely explained. We aimed to determine the effects of NOS inhibition by N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME), a NOS inhibitor, on NASH and CVD via lipid and cholesterol metabolism. METHODS: Stroke-prone spontaneously hypertensive rats were fed a high-fat and high-cholesterol diet for 8 weeks and administered L-NAME for the last 2 weeks. Following blood and tissue sampling, biochemical analysis, histopathological staining, quantitative RT-PCR analysis, and western blotting were performed. RESULTS: L-NAME markedly increased hepatic triglyceride (TG) and cholesterol levels by promoting TG synthesis and cholesterol absorption from the diet. L-NAME increased the mRNA levels of inflammatory markers and fibrotic areas in the liver. Cholesterol secretion from the liver was promoted in rats administered L-NAME, which increased serum cholesterol. L-NAME significantly increased the level of oxidative stress marker and lipid deposition in the arteries. CONCLUSIONS: NOS inhibition simultaneously aggravates NASH and atherosclerosis via hepatic lipid and cholesterol metabolism.

    DOI： 10.1007/s43440-022-00380-1

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  • Basic characteristics between mechanomyogram and muscle force during twitch and tetanic contractions in rat skeletal muscles. Reviewed International journal

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Shota Kumazaki, Mami Matsui, Hinako Nakayama, Sora Kirihara, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology   62   102627 - 102627   2022.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    The mechanomyogram (MMG) is a signal measured by various vibration sensors for slight vibrations induced by muscle contraction, and it reflects the muscle force during electrically induced-contraction or until 60%-70% maximum voluntary contraction, so the MMG is considered an alternative and novel measurement tool for muscle strength. We simultaneously measured the MMG and muscle force in the gastrocnemius (GC), vastus intermedius (VI), and soleus (SOL) muscles of rats. The muscle force was measured by attaching a hook to the tendon using a load cell, and the MMG was measured using a charged-coupled device-type displacement sensor at the middle of the target muscle. The MMG-twitch waveform was very similar to that of the muscle force; however, the half relaxation time and relaxation time (10%), which are relaxation parameters, were prolonged compared to those of the muscle force. The MMG amplitude correlated with the muscle force. Since stimulation frequencies that are necessary to evoke tetanic progression have a significant correlation with the twitch parameter, there is a close relationship between twitch and tetanus in the MMG signal. Therefore, we suggest that the MMG, which is electrically induced and detected by a laser displacement sensor, may be an alternative tool for measuring muscle strength.

    DOI： 10.1016/j.jelekin.2021.102627

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  • Bile acids aggravate nonalcoholic steatohepatitis and cardiovascular disease in SHRSP5/Dmcr rat model. Reviewed International journal

    Shusei Yamamoto, Ikumi Sato, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shota Kumazaki, Shang Ran, Satoshi Hirohata, Kazuya Kitamori, Yukio Yamori, Shogo Watanabe

    Experimental and molecular pathology   114   104437 - 104437   2020.6

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    BACKGROUND AND AIMS: Nonalcoholic steatohepatitis (NASH) is linked to an increased risk of cardiovascular disease, regardless of the risk factors in metabolic syndrome. However, the intermediary factors between NASH and cardiovascular disease are still unknown. A previous study revealed that serum and hepatic bile acid (BA) levels are increased in some NASH patients. We aimed to examine whether NASH and cardiovascular disease were aggravated by BA using an animal model. METHOD AND RESULTS: From 10 to 18 weeks of age, SHRSP5/Dmcr rats divided into 3 groups were fed 3 types of high-fat and high-cholesterol (HFC) diets which were changed in the cholic acid (CA) concentration (0%, 2%, or 4%). The nitro oxide synthase inhibition (L-NAME) was administered intraperitoneally from 16 to 18 weeks of age. The 4% CA groups showed the worst LV dysfunction and myocardial fibrosis, and demonstrated severe hepatic fibrosis and lipid depositions. In addition, a large amount of lipid accumulation was observed in the aortas of the 4% CA group, and NFκB and VCAM-1 gene expression levels were increased. These findings were not seen in the 0% CA group. CONCLUSION: In the SHRSP5/Dmcr rat model, NASH and cardiovascular disease were aggravated with increasing BAs concentrations in an HFC diet.

    DOI： 10.1016/j.yexmp.2020.104437

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  • Bile Acid Metabolism is an Intermediary Factor between Non-Alcoholic Steatohepatitis and Ischemic Heart Disease in SHRSP5/Dmcr Rats Reviewed International journal

    Shota Kumazaki, Mayu Nakamura, Shun Sasaki, Rina Tagashira, Nozomi Maruyama, Ikumi Sato, Shusei Yamamoto, Shang Ran, Shinichi Usui, Ryoko Shinohata, Takashi Ohtsuki, Satoshi Hirohata, Kazuya Kitamori, Mari Mori, Yukio Yamori, Shogo Watanabe

    Journal of Nutrition & Food Sciences   9 ( 4 )   2019.10

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    Language：English   Publishing type：Research paper (scientific journal)  

    The non-alcoholic steatohepatitis (NASH) increases the cardiovascular risk regardless of risk factors in metabolic syndrome. The stroke-prone (SP) spontaneously hypertensive rats (SHRSP5/Dmcr), fed a high-fat and -cholesterol (HFC) diet and administered Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) presented NASH and cardiovascular disease. However, the intermediary factors between NASH and cardiovascular risk are still unknown. We investigated whether bile acids (BAs) play an intermediary role between NASH and cardiovascular disease in SHRSP5/Dmcr rats. SHRSP5/Dmcr rats divided into 2 groups were fed an SP (non-NASH group, n=7) or HFC diet (NASH group, n=10) for 8 weeks. L-NAME was administered intraperitoneally in the final 2 weeks. In the
    NASH group, total BA levels were increased in both serum and liver; they aggravated the endothelial dysfunction in aorta, which is the first step to atherosclerosis, and activated the gene expression levels of cell adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1) in coronary artery. In particular, the nuclear factor-kappa B (NFkB) was increased in the NASH group in the coronary endothelial cells activated by high BA levels. We demonstrated that liver BAs aggravated steatosis and fibrosis and serum BA accelerated arteriosclerosis and ischemic heart disease via the classical pathway of NFkB in the endothelial cells. BA metabolism disorder may
    be an intermediary factor between NASH and cardiovascular risk in SHRSP5/Dmcr rats.

    DOI： 10.35248/2155-9600.19.9.1000763

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  • Non-alcoholic steatohepatitis aggravates nitric oxide synthase inhibition-induced arteriosclerosis in SHRSP5/Dmcr rat model. Reviewed International journal

    Shogo Watanabe, Shota Kumazaki, Shusei Yamamoto, Ikumi Sato, Kazuya Kitamori, Mari Mori, Yukio Yamori, Satoshi Hirohata

    International journal of experimental pathology   99 ( 6 )   282 - 294   2018.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    Non-alcoholic steatohepatitis (NASH) is linked to increased cardiovascular risk, independent of the broad spectrum of metabolic syndrome risk factors. Stroke-prone (SP) spontaneously hypertensive rats (SHRSP5/Dmcr) fed a high-fat and high-cholesterol (HFC) diet developed hepatic lesions similar to those in human NASH pathology. These rats simultaneously developed lipid deposits in the mesenteric arteries, cardiac fibrosis, endothelial dysfunction and left ventricle (LV) diastolic dysfunction. However, the intermediary factors between NASH and cardiovascular disease are still unknown. We investigated whether NASH aggravates nitric oxide (NO) synthase inhibition-induced arteriosclerosis in SHRSP5/Dmcr rats. Wistar Kyoto and SHRSP5/Dmcr rats were divided into 4 groups of 5 and fed the stroke-prone (SP) or HFC diets for 8 weeks. To induce NO synthase inhibition, Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME) mixed with drinking water was administered in the final 2 weeks. The NASH+L-NAME group demonstrated the following characteristics related to arteriosclerosis and myocardial ischaemia: (a) LV systolic dysfunction with asynergy, (b) replacement fibrosis caused by the shedding of cardiomyocytes and (c) arterial lipid deposition and coronary occlusion secondary to endothelial dysfunction. These characteristics were not observed in the NASH or non-NASH+L-NAME groups. The SHRSP5/Dmcr rat model demonstrates that NASH significantly aggravates cardiovascular risk.

    DOI： 10.1111/iep.12301

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MISC

  • ベタメタゾン添加OUMS-27による細胞外小胞のマトリックス分解酵素抑制効果

    井口和香, 安達加奈子, 岩本結, 中村早希, 佐藤生弥, ファルハナ ハシブ, 池村健太郎, ガブリエル オポク, 廣畑聡

    第96回日本生化学会大会   2023.11

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  • miR-150-5pを用いた、CEMIP発現抑制効果の検討

    平林沙江子, 池村健太郎, Opoku Gabriel, 高下蓮, Hasib Farhan, 井口和香, 佐藤生弥, 廣畑聡

    第96回日本生化学会大会   2023.11

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  • Effect of Stromal Vascular Fraction-Derived Extracellular Vesicles on Chondrocytic cells

    Farhana Hasib, Airi Nakano, Gabriel Opoku, Kentaro Ikemura, Saeko Hirabayashi, Ren Takashita, Nodoka Iguchi, Ikumi Sato, Satoshi Hirohata

    The 96th Annual Meeting of the Japanese Biochemical Society   2023.11

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  • Versican Distribution and Its Cleavage in Adamts1 Knockout Mouse Embryos

    Gabriel Opoku, Kentaro Ikemura, Omer Faruk Hatipoglu, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Iguchi Nodoka, Ikumi Sato, Eri Katsuyama, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP   2023.10

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  • Collagen Distribution in Mouse Embryo Abdominal Wall

    Kentaro Ikemura, Gabriel Opoku, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Nodoka Iguchi, Ikumi Sato, Eri Katsuyamma, Shogo Watanabe, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP   2023.10

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  • Osteopontin and CCR2 Are Involved in the inflammatory Cells in Non-alcoholic Steatohepatitis Model Rats

    Ikumi Sato, Ryosuke Ando, Rikuto Someya, Kurumi Matsuki, Kentaro Ikemura, Gabriel Opoku, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Nodoka Iguchi, Eri Katsuyama, Shusei Yamamoto, Shogo Watanabe, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP   2023.10

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  • 薬剤添加による細胞外小胞のマトリックス分解酵素抑制効果の比較

    井口和香, 佐藤生弥, 安達嘉奈子, 岩本結衣, 中村早希, 中野愛理, 山元修成, 渡辺 彰吾, 廣畑聡

    第17回日本臨床検査学教育学会学術大会   2023.8

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  • マクロファージの分極とオステオポンチン /CCR2 の発現 －非アルコール性脂 肪肝炎線維化への関与－

    佐藤生弥, 安藤亮典, 池村健太郎, Gabriel Opoku, 中野愛理, 高下蓮, 平林沙江子, Farhana Hasib, 井口和香, 勝山惠理, 廣畑聡

    第55回日本結合組織学会学術大会   2023.6

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  • 胎生後期におけるマウス腹壁でのバーシカンとコラーゲンの分布

    池村健太郎, ガブリエル・オポク, 高下蓮, 平林沙江子, ファルハナ・ハシブ, 井口和香, 佐藤生弥, 勝山恵理, 廣畑聡

    2023.6

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  • HEK-293 由来細胞外小胞の軟骨細胞と滑膜細胞への取り込みの検討

    高下蓮, 池村健太郎, Opoku Gabrie, 鶴川しほろ, 平林沙江子, 井口和香, Farhana Hasi, 佐藤生弥, 古松毅之, 西田圭一郎, 安藤満, 秋吉一成, 廣畑聡

    第55回日本結合組織学会学術大会   2023.6

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  • タンパク質分解性バーシカン分解と皮筋層の発達との関連

    ガブリエル・オポク, 池村健太郎, 高下蓮, 平林沙江子, ファルハナ・ハシブ, 井口和香, 佐藤生弥, 勝山恵理, 廣畑聡

    第55回日本結合組織学会学術大会   2023.6

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  • miR-150とCEMIP mRNAとの結合性に関する検討

    平林沙江子, 浦木美能理, 池村健太郎, Gabriel Opoku, 高下蓮, Farhana Hasib, 佐藤生弥, 勝山恵理, 廣畑聡

    第55回日本結合組織学会学術大会   2023.6

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  • 間質血管画分由来の細胞外分泌小胞がもつマトリックスメタロプロテアーゼ 13 に対する効果

    Farhana Hasib, 中野愛理, 池村健太郎, Gabriel Opoku, 安藤亮典, 高下蓮, 平林沙江子, 佐藤生弥, 勝山惠理, 廣畑聡

    第55回日本結合組織学会学術大会   2023.6

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  • Suppression of the NO/AMPK Pathway Aggravates Non-Alcoholic Steatohepatitis and Cardiovascular Disease via Abnormal Lipid Metabolism in SHRSP5/Dmcr rat

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Hinako Nakayama, Sora Kirihara, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

    32nd Conference of the Asian Pacific Association for the Study of the Liver (APASL 2023)   2023.2

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  • 鉄代謝はNASHと動脈硬化を結ぶ新たなリスク因子になりうるか

    本間宏基, 桐原空, 中山日菜子, 柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 山元修成, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   54th   2022

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  • フルクトース負荷による尿酸上昇がNASHと動脈硬化に及ぼす影響

    藤井萌, 柿本麻衣, 山元修成, 佐藤生弥, 本間宏基, 小松千尋, 奥川友葉, 柴田桃里, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   53rd   2021

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  • XO阻害薬フェブキソスタットによる抗酸化作用は肝臓・血管系を保護する

    柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 本間宏基, 奥川友葉, 柴田桃里, 小松千尋, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   53rd   2021

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  • 新規LXRβアゴニストであるウアバゲニンを用いた動脈脂質沈着に対する改善効果の検討

    山元修成, 佐藤生弥, 柿本麻衣, 藤井萌, 松井麻実, 高橋侑子, 弥勒院佳奈, RAN Shang, 田村理, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   52nd   2020

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  • オベチコール酸はSHRSP5/Dmcrラットにおける非アルコール性脂肪肝炎とアテローム性動脈硬化症を改善する

    佐藤生弥, 山元修成, 柿本麻衣, 藤井萌, 松井麻実, 高橋侑子, 弥勒院佳奈, RAN Shang, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   52nd   2020

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  • 非アルコール性脂肪肝炎と心血管疾患を増悪させる仲介因子としての胆汁酸の役割

    佐藤生弥, 熊崎章太, 山元修成, 福濱那月, 秋山菜摘, 酒井美玖, シャン ラン, 廣畑聡, 渡辺彰吾

    日本動脈硬化学会総会・学術集会プログラム・抄録集(Web)   51st   2019

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  • 非アルコール性脂肪肝炎において心血管疾患を増悪する仲介因子となり得る胆汁酸代謝

    山元修成, 佐藤生弥, 秋山菜摘, 酒井美玖, 福濱那月, SHANG Ran, 廣畑聡, 渡邊彰吾

    日本循環薬理学会口演要旨集   29th   2019

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Presentations

  • Effect of Stromal Vascular Fraction-Derived Extracellular Vesicles on Chondrocytic cells

    Farhana Hasib, Airi Nakano, Gabriel Opoku, Kentaro Ikemura, Saeko Hirabayashi, Ren Takashita, Nodoka Iguchi, Ikumi Sato, Satoshi Hirohata

    The 96th Annual Meeting of the Japanese Biochemical Society  2023.11.1 

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    Event date： 2023.10.31 - 2023.11.2

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  • MiR-150-5p regulates the CEMIP expression in chondrosarcoma cells

    Saeko Hirabayashi, Kentaro Ikemura, Gabriel Opoku, Ren Takashita, Farhana Hasib, Nodoka Iguchi, Ikumi Sato, Satoshi Hirohata

    2023.11.1 

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    Event date： 2023.10.31 - 2023.11.2

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  • Inhibition of matrix degrading enzymes in extracellular vesicles by betamethasone

    Nodoka Iguchi, Kanako Adachi, Yui Iwamoto, Saki Nakamura, Ikymi Sato, Farhana Hasib, Kentaro Ikemura, Gabriel Opoku, Satoshi Hirohata

    2023.11.1 

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    Event date： 2023.10.31 - 2023.11.2

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  • Osteopontin and CCR2 Are Involved in the inflammatory Cells in Non-alcoholic Steatohepatitis Model Rats

    Ikumi Sato, Ryosuke Ando, Rikuto Someya, Kurumi Matsuki, Kentaro Ikemura, Gabriel Opoku, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Nodoka Iguchi, Eri Katsuyama, Shusei Yamamoto, Shogo Watanabe, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP  2023.10.24 

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    Event date： 2023.10.22 - 2023.10.25

    File： 2023-Joint-Meeting-Scientific-Program.pdf

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  • Versican Distribution and Its Cleavage in Adamts1 Knockout Mouse Embryos

    Gabriel Opoku, Kentaro Ikemura, Omer Faruk Hatipoglu, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Iguchi Nodoka, Ikumi Sato, Eri Katsuyama, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP  2023.10.24 

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    Event date： 2023.10.22 - 2023.10.25

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  • Collagen Distribution in Mouse Embryo Abdominal Wall

    Kentaro Ikemura, Gabriel Opoku, Ren Takashita, Saeko Hirabayashi, Farhana Hasib, Nodoka Iguchi, Ikumi Sato, Eri Katsuyamma, Shogo Watanabe, Satoshi Hirohata

    Tissue, Matrix, and Pathobiology: Joint Meeting of ASMB, HCS, and ASIP  2023.10.23 

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    Event date： 2023.10.22 - 2023.10.25

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  • 薬剤添加による細胞外小胞のマトリックス分解酵素抑制効果の比較

    井口和香, 佐藤生弥, 安達嘉奈子, 岩本結衣, 中村早希, 中野愛理, 山元修成, 渡辺 彰吾, 廣畑聡

    第17回日本臨床検査学教育学会学術大会  2023.8.23 

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  • Distribution of versican and collagen in mouse abdominal wall at the late embryonic stage

    Ikemura K, Gabriel O, Takashita R, Hirabayashi S, Farhana H, Iguchi W, Ookubo S, Sato I, Katsuyama E, Watanabe S, Hirohata S

    Gordon Research Conference (Collagen) 

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    Event date： 2023.7.9 - 2023.7.14

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  • マクロファージの分極とオステオポンチン /CCR2 の発現 －非アルコール性脂 肪肝炎線維化への関与－

    佐藤生弥, 安藤亮典, 池村健太郎, Gabriel Opoku, 中野愛理, 高下蓮, 平林沙江子, Farhana Hasib, 井口和香, 勝山惠理, 廣畑聡

    第55回日本結合組織学会学術大会  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

    File： 結合組織学会プログラム.pdf

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  • The relationship between proteolytic versican degradation and panniculus carnosus development demusclededevelopment

    The 55th Annual Meeting of the Japanese Society for Matrix Biology and Medicine  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

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  • MiR-150 binds to the CEMIP-3’UTR sequence

    Hirabayashi S, Uraki S, Ikemura K, Opoku G, Takashita R, Hasib F, Sato I, Katuyama E, Hirohata S

    The 55th Annual Meeting of the Japanese Society for Matrix Biology and Medicine  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

    File： 結合組織学会プログラム.pdf

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  • 胎生後期におけるマウス腹壁でのバーシカンとコラーゲンの分布

    池村健太郎, ガブリエル・オポク, 高下蓮, 平林沙江子, ファルハナ・ハシブ, 井口和香, 佐藤生弥, 勝山恵理, 廣畑聡

    第55回日本結合組織学会学術大会  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

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  • 間質血管画分由来の細胞外分泌小胞がもつマトリックスメタロプロテアーゼ 13 に対する効果

    Farhana Hasib, 中野愛理, 池村健太郎, Gabriel Opoku, 安藤亮典, 高下蓮, 平林沙江子, 佐藤生弥, 勝山惠理, 廣畑聡

    第55回日本結合組織学会学術大会  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

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  • HEK-293-derived EVs was uptaken by chondrocytes and synoviocytes

    The 55th Annual Meeting of the Japanese Society for Matrix Biology and Medicine  2023.6.24 

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    Event date： 2023.6.24 - 2023.6.25

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  • Suppression of the NO/AMPK Pathway Aggravates Non-Alcoholic Steatohepatitis and Cardiovascular Disease via Abnormal Lipid Metabolism in SHRSP5/Dmcr rat

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Hinako Nakayama, Sora Kirihara, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

    32nd Conference of the Asian Pacific Association for the Study of the Liver (APASL 2023) 

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    Event date： 2023.2.15 - 2023.2.19

    Language：English   Presentation type：Poster presentation  

    Venue：Taipei  

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  • 鉄代謝は非アルコール性脂肪肝炎と動脈硬化を結ぶ新たなリスク因子になりうるか

    本間宏基, 桐原空, 中山日菜子, 柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 廣畑聡, 渡辺彰吾

    第54回日本動脈硬化学会総会・学術集会  2022.7.23 

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    Event date： 2022.7.23 - 2022.7.24

    Language：Japanese   Presentation type：Poster presentation  

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  • フルクトース負荷による尿酸上昇がNASHと動脈硬化に及ぼす影響

    藤井萌, 柿本麻衣, 山元修成, 佐藤生弥, 本間宏基, 小松千尋, 奥川友葉, 柴田桃里, 廣畑聡, 渡辺彰吾

    第53回日本動脈硬化学会総会・学術集会 

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    Event date： 2021.10.23 - 2021.10.24

    Language：Japanese   Presentation type：Poster presentation  

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  • XO阻害薬フェブキソスタットによる抗酸化作用は肝臓・血管系を保護する

    柿本麻衣, 藤井萌, 佐藤生弥, 山元修成, 本間宏基, 奥川友葉, 柴田桃里, 小松千尋, 廣畑聡, 渡辺彰吾

    第53回日本動脈硬化学会総会・学術集会 

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    Event date： 2021.10.23 - 2021.10.24

    Language：Japanese   Presentation type：Poster presentation  

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  • Effect of Elevated Uric Acid by Fructose Overload on NASH and Atherosclerosis

    Moe Fujii, Mai Kakimoto, Shusei Yamamoto, Ikumi Sato, Koki Honma, Chihiro Komatsu, Tomoha Okugawa, Momori Shibata, Satoshi Hirohata, Shogo Watanabe

    The 10th International Congress on Lipid & Atherosclerosis (ICoLA)  2021.9.10 

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    Event date： 2021.9.10 - 2021.9.11

    Language：English   Presentation type：Oral presentation (general)  

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  • Antioxidant Action of Xanthine Oxidase Inhibitor Febuxostat Protects Liver and Blood Vascular System

    Mai Kakimoto, Moe Fujii, Ikumi Sato, Shusei Yamamoto, Koki Honma, Tomoha Okugawa, Momori Shibata, Chihiro Komatsu, Satoshi Hirohata, Shogo Watanabe

    The 10th International Congress on Lipid & Atherosclerosis (ICoLA) 

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    Event date： 2021.9.10 - 2021.9.11

    Language：English  

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  • The Novel Liver X Receptor beta Agonist, Ouabagenin, Prevent Arterial Lipid Deposition in SHRSP5/Dmcr Rat

    Shusei Yamamoto, Ikumi Satoh, Mai Kakimoto, Moe Fujii, Mami Matsui, Yuko Takahashi, Kana Mirokuin, Shang Ran, Satoru Tamura, Satoshi Hirohata, Shogo Watanabe

    The 88th European Atherosclerosis Society (EAS) Congress 

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    Event date： 2020.10.4 - 2020.10.7

    Language：English  

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  • Obeticholic acid ameliorates Non-alcoholic steatohepatitis and atherosclerosis in SHRSP5/Dmcr rats

    Ikumi Satoh, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Mami Matsui, Yuko Takahashi, Kana Mirokuin, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    The 88th European Atherosclerosis Society (EAS) Congress 

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    Event date： 2020.10.4 - 2020.10.7

    Language：English  

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  • 新規LXRβアゴニストであるウアバゲニンを用いた動脈脂質沈着に対する改善効果の検討

    山元修成, 佐藤生弥, 柿本麻衣, 藤井萌, 松井麻実, 髙橋侑子, 弥勒院佳奈, Shang Ran, 田村理, 廣畑聡, 渡辺彰吾

    第52回日本動脈硬化学会総会・学術集会 

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    Event date： 2020.7.17 - 2020.7.31

    Language：Japanese  

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  • オベチコール酸はSHRSP5/Dmcrラットにおける非アルコール性脂肪肝炎とアテローム性動脈硬化症を改善する

    佐藤生弥, 山元修成, 柿本麻衣, 藤井萌, 松井麻実, 髙橋侑子, 弥勒院佳奈, Shang Ran, 廣畑聡, 渡辺彰吾

    第52回日本動脈硬化学会総会・学術集会 

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    Event date： 2020.7.17 - 2020.7.31

    Language：English  

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  • 非アルコール性脂肪肝炎において心血管疾患を増悪する仲介因子となり得る胆汁酸代謝

    山元修成, 佐藤生弥, 秋山菜摘, 酒井美玖, 福濱那月, Shang Ran, 廣畑聡, 渡辺彰吾

    第55回高血圧関連疾患モデル学会  2019.11.29 

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    Event date： 2019.11.29 - 2019.11.30

    Presentation type：Oral presentation (general)  

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  • Bile Acids Aggravate Non-alcoholic Steatohepatitis and Cardiovascular Disease in SHRSP5/Dmcr

    Ikumi Satoh, Shusei Yamamoto, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shang Ran, Shota Kumazaki, Satoshi Hirohata, Shogo Watanabe

    The 8th International Congress on Lipid & Atherosclerosis (ICoLA)  2019.9.6 

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    Event date： 2019.9.5 - 2019.9.7

    Language：English   Presentation type：Poster presentation  

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  • Bile Acid Metabolism Mediates between Nonalcoholic Steatohepatitis and Cardiovascular Disease

    Shusei Yamamoto, Ikumi Sato, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shota Kumazaki, Shang Ran, Satoshi Hirohata, Shogo Watanabe

    The 8th International Congress on Lipid & Atherosclerosis (ICoLA) 

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    Event date： 2019.9.5 - 2019.9.7

    Language：English   Presentation type：Poster presentation  

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  • 非アルコール性脂肪肝炎と心血管疾患を増悪させる仲介因子としての胆汁酸の役割

    佐藤生弥, 熊崎章太, 山元修成, 福濱那月, 秋山菜摘, 酒井美玖, Shang Ran, 廣畑聡, 渡辺彰吾

    第51回日本動脈硬化学会総会・学術集会  2019.7.11 

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    Event date： 2019.7.11 - 2019.7.12

    Presentation type：Poster presentation  

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Awards

  • Best Poster Award

    2023.2   32nd Conference of the Asian Pacific Association for the Study of the Liver (APASL2023)   Suppression of the NO/AMPK Pathway Aggravates Non-Alcoholic Steatohepatitis and Cardiovascular Disease via Abnormal Lipid Metabolism in SHRSP5/Dmcr

    Ikumi Sato, Shusei Yamamoto, Mai Kakimoto, Moe Fujii, Koki Honma, Hinako Nakayama, Sora Kirihara, Shinichi Usui, Ryoko Shinohata, Kazuya Kitamori, Satoshi Hirohata, Shogo Watanabe

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  • Travel Grant

    2019.9   International Congress on Lipid & Atherosclerosis (ICoLA)   Bile Acids Aggravate Non-alcoholic Steatohepatitis and Cardiovascular Disease in SHRSP5/Dmcr

    Ikumi Sato, Shusei Yamamoto, Natsuki Fukuhama, Natsumi Akiyama, Miku Sakai, Shang Ran, Shota Kumazaki, Satoshi Hirohata, Shogo Watanabe

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Research Projects

  • プレコンディショニング下の間葉系幹細胞由来エクソソームによる抗動脈硬化作用

    Grant number：23K16796  2023.04 - 2025.03

    日本学術振興会  科学研究費助成事業  若手研究

    佐藤 生弥

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    Grant amount：\4680000 （ Direct expense: \3600000 、 Indirect expense：\1080000 ）

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  • キサンチン酸化還元酵素阻害薬による痩せ型NASH および動脈硬化への治療効果

    2022.12 - 2024.03

    公益財団法人 痛風・尿酸財団  2022年度痛風・尿酸財団研究助成 

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    Authorship：Coinvestigator(s) 

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Class subject in charge

  • Exercise of Team Medical Activities （2023academic year） 1st and 2nd semester  - その他

  • Laboratory Exercise in Laboratory Immunology （2023academic year） Second semester  - 水3～8,木3～8

  • Medical Safety Management science （2023academic year） 1st semester  - 月2～3

  • Laboratory Management （2023academic year） 1st semester  - 月7～8

  • Laboratory Exercise in Clinical Physiology （2023academic year） 3rd and 4th semester  - [第３学期]火1～8,水3～8, [第４学期]火1～8

  • Laboratory Exercise in Clinical Chemistry （2023academic year） Third semester  - 月1～6,木3～8

  • Laboratory Science Exercise （2023academic year） 2nd and 3rd semester  - [第２学期]火7, [第３学期]月7

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