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245 results on '"Imai, Hirotaka"'

5. Oxidative Metabolism as a Cause of Lipid Peroxidation in the Execution of Ferroptosis.

Author

Fujii, Junichi and Imai, Hirotaka

Subjects
*LIPID metabolism, *KREBS cycle, *PEROXIDATION, *GLUTATHIONE peroxidase, *AMINO group, *RADICALS (Chemistry)
Abstract

Ferroptosis is a type of nonapoptotic cell death that is characteristically caused by phospholipid peroxidation promoted by radical reactions involving iron. Researchers have identified many of the protein factors that are encoded by genes that promote ferroptosis. Glutathione peroxidase 4 (GPX4) is a key enzyme that protects phospholipids from peroxidation and suppresses ferroptosis in a glutathione-dependent manner. Thus, the dysregulation of genes involved in cysteine and/or glutathione metabolism is closely associated with ferroptosis. From the perspective of cell dynamics, actively proliferating cells are more prone to ferroptosis than quiescent cells, which suggests that radical species generated during oxygen-involved metabolism are responsible for lipid peroxidation. Herein, we discuss the initial events involved in ferroptosis that dominantly occur in the process of energy metabolism, in association with cysteine deficiency. Accordingly, dysregulation of the tricarboxylic acid cycle coupled with the respiratory chain in mitochondria are the main subjects here, and this suggests that mitochondria are the likely source of both radical electrons and free iron. Since not only carbohydrates, but also amino acids, especially glutamate, are major substrates for central metabolism, dealing with nitrogen derived from amino groups also contributes to lipid peroxidation and is a subject of this discussion. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Lipid Peroxidation-Dependent Cell Death Regulated by GPx4 and Ferroptosis

Author

Imai, Hirotaka, Matsuoka, Masaki, Kumagai, Takeshi, Sakamoto, Taro, Koumura, Tomoko, Compans, Richard W, Series editor, Honjo, Tasuku, Series editor, Oldstone, Michael B. A., Series editor, Vogt, Peter K., Series editor, Malissen, Bernard, Series editor, Aktories, Klaus, Series editor, Kawaoka, Yoshihiro, Series editor, Rappuoli, Rino, Series editor, Galan, Jorge E., Series editor, Ahmed, Rafi, Series editor, Palme, Klaus, Series editor, Casadevall, Arturo, Series editor, Garcia-Sastre, Adolfo, Series editor, Nagata, Shigekazu, editor, and Nakano, Hiroyasu, editor

Published
2017
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10. Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis

Author

Yoshida, Masahiro, Minagawa, Shunsuke, Araya, Jun, Sakamoto, Taro, Hara, Hiromichi, Tsubouchi, Kazuya, Hosaka, Yusuke, Ichikawa, Akihiro, Saito, Nayuta, Kadota, Tsukasa, Sato, Nahoko, Kurita, Yusuke, Kobayashi, Kenji, Ito, Saburo, Utsumi, Hirohumi, Wakui, Hiroshi, Numata, Takanori, Kaneko, Yumi, Mori, Shohei, Asano, Hisatoshi, Yamashita, Makoto, Odaka, Makoto, Morikawa, Toshiaki, Nakayama, Katsutoshi, Iwamoto, Takeo, Imai, Hirotaka, and Kuwano, Kazuyoshi

Published
2019
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13. Ethoxyquin is a Competent Radical-Trapping Antioxidant for Preventing Ferroptosis in Doxorubicin Cardiotoxicity

Author

Tadokoro, Tomonori, primary, Ikeda, Masataka, additional, Abe, Ko, additional, Ide, Tomomi, additional, Miyamoto, Hiroko Deguchi, additional, Furusawa, Shun, additional, Ishimaru, Kosei, additional, Watanabe, Masatsugu, additional, Ishikita, Akihito, additional, Matsushima, Shouji, additional, Koumura, Tomoko, additional, Yamada, Ken-ichi, additional, Imai, Hirotaka, additional, and Tsutsui, Hiroyuki, additional

Published
2022
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14. Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis

Author

Abe, Ko, primary, Ikeda, Masataka, additional, Ide, Tomomi, additional, Tadokoro, Tomonori, additional, Miyamoto, Hiroko Deguchi, additional, Furusawa, Shun, additional, Tsutsui, Yoshitomo, additional, Miyake, Ryo, additional, Ishimaru, Kosei, additional, Watanabe, Masatsugu, additional, Matsushima, Shouji, additional, Koumura, Tomoko, additional, Yamada, Ken-ichi, additional, Imai, Hirotaka, additional, and Tsutsui, Hiroyuki, additional

Published
2022
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19. Characterization of H7N9 influenza A viruses isolated from humans

Author

Watanabe, Tokiko, Kiso, Maki, Fukuyama, Satoshi, Nakajima, Noriko, Imai, Masaki, Yamada, Shinya, Murakami, Shin, Yamayoshi, Seiya, Iwatsuki-Horimoto, Kiyoko, Sakoda, Yoshihiro, Takashita, Emi, McBride, Ryan, Noda, Takeshi, Hatta, Masato, Imai, Hirotaka, Zhao, Dongming, Kishida, Noriko, Shirakura, Masayuki, de Vries, Robert P., Shichinohe, Shintaro, Okamatsu, Masatoshi, Tamura, Tomokazu, Tomita, Yuriko, Fujimoto, Naomi, Goto, Kazue, Katsura, Hiroaki, Kawakami, Eiryo, Ishikawa, Izumi, Watanabe, Shinji, Ito, Mutsumi, Sakai-Tagawa, Yuko, Sugita, Yukihiko, Uraki, Ryuta, Yamaji, Reina, Eisfeld, Amie J., Zhong, Gongxun, Fan, Shufang, Ping, Jihui, Maher, Eileen A., Hanson, Anthony, Uchida, Yuko, Saito, Takehiko, Ozawa, Makoto, Neumann, Gabriele, Kida, Hiroshi, Odagiri, Takato, Paulson, James C., Hasegawa, Hideki, Tashiro, Masato, and Kawaoka, Yoshihiro

Published
2013
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23. In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses

Author

Itoh, Yasushi, Shinya, Kyoko, Kiso, Maki, Watanabe, Tokiko, Sakoda, Yoshihiro, Hatta, Masato, Muramoto, Yukiko, Tamura, Daisuke, Sakai-Tagawa, Yuko, Noda, Takeshi, Sakabe, Saori, Imai, Masaki, Hatta, Yasuko, Watanabe, Shinji, Li, Chengjun, Yamada, Shinya, Fujii, Ken, Murakami, Shin, Imai, Hirotaka, Kakugawa, Satoshi, Ito, Mutsumi, Takano, Ryo, Iwatsuki-Horimoto, Kiyoko, Shimojima, Masayuki, Horimoto, Taisuke, Goto, Hideo, Takahashi, Kei, Makino, Akiko, Ishigaki, Hirohito, Nakayama, Misako, Okamatsu, Masatoshi, Takahashi, Kazuo, Warshauer, David, Shult, Peter A., Saito, Reiko, Suzuki, Hiroshi, Furuta, Yousuke, Yamashita, Makoto, Mitamura, Keiko, Nakano, Kunio, Nakamura, Morio, Brockman-Schneider, Rebecca, Mitamura, Hiroshi, Yamazaki, Masahiko, Sugaya, Norio, Suresh, M., Ozawa, Makoto, Neumann, Gabriele, Gern, James, Kida, Hiroshi, Ogasawara, Kazumasa, and Kawaoka, Yoshihiro

Published
2009
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30. Inhibition of lipid peroxidation during the reproductive period extends the lifespan of

Author

Sakamoto, Taro, Maebayashi, Kana, Tsunoda, Yuka, and Imai, Hirotaka

Subjects
Original Article
Abstract

Glutathione peroxidase 4 (GPx4) is a unique antioxidant enzyme that directly reduces the phospholipid hydroperoxides (PLOOH) generated in biomembranes using glutathione as the reductant. We have previously reported that the Caenorhabditis elegans gpx-quad mutant, which lacks all homologous genes of GPx4 has a reduced lifespan compared with the wild-type. However, the mechanisms underlying the lifespan reduction remain unclear. By monitoring the change in PLOOH production with age, we found that PLOOH was elevated in the gpx-quad mutants compared with the wild-type during the reproductive period. Administration of vitamin E not only reduced the PLOOH content but also prolonged the lifespan of the gpx-quad mutants. In contrast, vitamin C did not extend the lifespan of the gpx-quad mutants. Interestingly, we found that the inhibition of lipid peroxidation by vitamin E during 5 to 10 days after hatching is important to extend the lifespan of C. elegans. These results suggest that production of PLOOH during the reproductive period strongly influences the lifespan of C. elegans.

Published
2019

34. Involvement of GPx4-Regulated Lipid Peroxidation in Idiopathic Pulmonary Fibrosis Pathogenesis

Author

Tsubouchi, Kazuya, primary, Araya, Jun, additional, Yoshida, Masahiro, additional, Sakamoto, Taro, additional, Koumura, Tomoko, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Kadota, Tsukasa, additional, Kurita, Yusuke, additional, Kobayashi, Kenji, additional, Ito, Saburo, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Mori, Shohei, additional, Asano, Hisatoshi, additional, Matsudaira, Hideki, additional, Ohtsuka, Takashi, additional, Nakayama, Katsutoshi, additional, Nakanishi, Yoichi, additional, Imai, Hirotaka, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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35. Pulmonary phagocyte-derived NPY controls the pathology of severe influenza virus infection

Author

Fujiwara, Seiki, primary, Hoshizaki, Midori, additional, Ichida, Yu, additional, Lex, Dennis, additional, Kuroda, Etsushi, additional, Ishii, Ken J., additional, Magi, Shigeyuki, additional, Okada, Mariko, additional, Takao, Hiroyuki, additional, Gandou, Masahiro, additional, Imai, Hirotaka, additional, Hara, Ryujiro, additional, Herzog, Herbert, additional, Yoshimura, Akihiko, additional, Okamura, Hitoshi, additional, Penninger, Josef M., additional, Slutsky, Arthur S., additional, Uhlig, Stefan, additional, Kuba, Keiji, additional, and Imai, Yumiko, additional

Published
2018
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39. Diversity of Influenza A(H5N1) Viruses in Infected Humans, Northern Vietnam, 2004–2010

Author

Imai, Hirotaka, primary, Dinis, Jorge M., additional, Zhong, Gongxun, additional, Moncla, Louise H., additional, Lopes, Tiago J.S., additional, McBride, Ryan, additional, Thompson, Andrew J., additional, Peng, Wenjie, additional, Le, Mai thi Q., additional, Hanson, Anthony, additional, Lauck, Michael, additional, Sakai-Tagawa, Yuko, additional, Yamada, Shinya, additional, Eggenberger, Julie, additional, O’Connor, David H., additional, Suzuki, Yasuo, additional, Hatta, Masato, additional, Paulson, James C., additional, Neumann, Gabriele, additional, Friedrich, Thomas C., additional, and Kawaoka, Yoshihiro, additional

Published
2018
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46. High‐level expression of STING restricts susceptibility to HBV by mediating type III IFN induction.

Author

Dansako, Hiromichi, Imai, Hirotaka, Ueda, Youki, Satoh, Shinya, Shimotohno, Kunitada, and Kato, Nobuyuki

Abstract

Hepatitis B virus (HBV) is a hepatotropic DNA virus causing hepatic diseases such as chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. To study HBV, human hepatoma HepG2 cells are currently used as an HBV infectious cell culture model worldwide. HepG2 cells exhibit susceptibility to HBV by exogenously expressing sodium taurocholate cotransporting polypeptide (NTCP). We herein demonstrated that human immortalized hepatocyte NKNT‐3 cells exhibited susceptibility to HBV by exogenously expressing NTCP (NKNT‐3/NTCP cells). By comparing cyclic GMP‐AMP synthetase (cGAS)‐stimulator of interferon genes (STING) signaling pathway in several NKNT‐3/NTCP cell‐derived cell clones, we found that STING was highly expressed in cell clones exhibiting resistance but not susceptibility to HBV. High‐level expression of STING was implicated in HBV‐triggered induction of type III IFN and a pro‐inflammatory cytokine, IL‐6. In contrast, RNAi‐mediated knockdown of STING inhibited type III IFN induction and restored the levels of HBV total transcript in an HBV‐infected cell clone exhibiting resistance to HBV. These results suggest that STING regulates susceptibility to HBV by its expression levels. STING may thus be a novel target for anti‐HBV strategies. [ABSTRACT FROM AUTHOR]

Published
2019
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47. Secreted d‐aspartate oxidase functions in C. elegans reproduction and development.

Author

Saitoh, Yasuaki, Katane, Masumi, Miyamoto, Tetsuya, Sekine, Masae, Sakamoto, Taro, Imai, Hirotaka, and Homma, Hiroshi

Subjects
ENZYMES, GENE expression, CAENORHABDITIS elegans, MOLECULAR biology, METHIONINE, ENDOCRINE glands
Abstract

d‐Aspartate oxidase (DDO) is a degradative enzyme that acts stereospecifically on free acidic D‐amino acids such as d‐aspartate and d‐glutamate. d‐Aspartate plays an important role in regulating neurotransmission, developmental processes, hormone secretion, and reproductive functions in mammals. In contrast, the physiological role of d‐glutamate in mammals remains unclear. In Caenorhabditis elegans, the enzyme responsible for in vivo metabolism of d‐glutamate is DDO‐3, one of the three DDO isoforms, which is also required for normal self‐fertility, hatching, and lifespan. In general, eukaryotic DDOs localize to subcellular peroxisomes in a peroxisomal targeting signal type 1 (PTS1)‐dependent manner. However, DDO‐3 does not contain a PTS1, but instead has a putative N‐terminal signal peptide (SP). In this study, we found that DDO‐3 is a secreted DDO, the first such enzyme to be described in eukaryotes. In hermaphrodites, DDO‐3 was secreted from the proximal gonadal sheath cells in a SP‐dependent manner and transferred to the oocyte surface. In males, DDO‐3 was secreted from the seminal vesicle into the seminal fluid in a SP‐dependent manner during mating with hermaphrodites. In both sexes, DDO‐3 was secreted from the cells where it was produced into the body fluid and taken up by scavenger coelomocytes. Full‐length DDO‐3 transgene rescued all phenotypes elicited by the deletion of ddo‐3, whereas a DDO‐3 transgene lacking the putative SP did not. Together, these results indicate that secretion of DDO‐3 is essential for its physiological functions. Eukaryotic d‐aspartate oxidase (DDO) is an enzyme that stereospecifically degrades free acidic d‐amino acids and is usually localized to the peroxisome. Saitoh et al. now describe the first secreted eukaryotic DDO in C. elegans, DDO‐3, and demonstrate that secretion of DDO‐3 is essential for normal fertility, hatching, lifespan, and nose touch response. [ABSTRACT FROM AUTHOR]

Published
2019
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