Kana Miyamoto
Keio University
64 Papers
206 Citations
Kana Miyamoto is an academic researcher from Keio University. The author has contributed to research in topics: Osteoclast & Osteoporosis. The author has an hindex of 26, co-authored 56 publications. Previous affiliations of Kana Miyamoto include Toho University & Kumamoto University.
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Papers
Stat3 as a potential therapeutic target for rheumatoid arthritis
Takatsugu Oike,Yuiko Sato,Tami Kobayashi,Kana Miyamoto,Satoshi Nakamura,Yosuke Kaneko,Shu Kobayashi,Kengo Harato,Hideyuki Saya,Morio Matsumoto,Masaya Nakamura,Yasuo Niki,Takeshi Miyamoto +12 more
TL;DR: Evidence is provided that signal transducer and activator of transcription 3 (Stat3) promotes inflammation and joint erosion in a mouse model of arthritis, suggesting that Stat3 inhibitors may serve as promising drugs for RA therapy.
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TNFα promotes osteosarcoma progression by maintaining tumor cells in an undifferentiated state.
Tomoaki Mori,Yuiko Sato,Kana Miyamoto,Tami Kobayashi,Takatsune Shimizu,Hiroya Kanagawa,Eri Katsuyama,Atsuhiro Fujie,Wu Hao,Toshimi Tando,Ryotaro Iwasaki,Hiromasa Kawana,Hideo Morioka,Morio Matsumoto,Hideyuki Saya,Yoshiaki Toyama,Takeshi Miyamoto +16 more
TL;DR: Inflammatory cytokines are required to promote tumorigenesis even in mutation-induced tumors, and TNFα/IL-1 and ERK may represent therapeutic targets for osteosarcoma.
Smad2/3 Proteins Are Required for Immobilization-induced Skeletal Muscle Atrophy
Toshimi Tando,Akiyoshi Hirayama,Mitsuru Furukawa,Yuiko Sato,Tami Kobayashi,Atsushi Funayama,Arihiko Kanaji,Wu Hao,Ryuichi Watanabe,Mayu Morita,Takatsugu Oike,Kana Miyamoto,Tomoyoshi Soga,Masatoshi Nomura,Akihiko Yoshimura,Masaru Tomita,Morio Matsumoto,Masaya Nakamura,Yoshiaki Toyama,Takeshi Miyamoto +19 more
TL;DR: It is shown that skeletal muscle immobilization elevates Smad2/3 protein but not mRNA levels in muscle, promoting atrophy, and myostatin, which negatively regulates muscle hypertrophy, is dispensable for denervation-induced muscle atrophy and Smad 2/3protein accumulation.
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Elevation of pro-inflammatory cytokine levels following anti-resorptive drug treatment is required for osteonecrosis development in infectious osteomyelitis.
Mayu Morita,Ryotaro Iwasaki,Yuiko Sato,Tami Kobayashi,Ryuichi Watanabe,Takatsugu Oike,Satoshi Nakamura,Yosuke Keneko,Kana Miyamoto,Kazuyuki Ishihara,Yoichiro Iwakura,Ken Ishii,Morio Matsumoto,Masaya Nakamura,Hiromasa Kawana,Taneaki Nakagawa,Takeshi Miyamoto +16 more
TL;DR: Administration of anti-resorptive agents such as the bisphosphonate alendronate accelerates osteonecrosis promoted by infectious osteomyelitis, and demonstrates that TNFα-, IL-1α/β- or IL-6-deficient mice as well as wild-type mice administered a TNFβ-inhibitor were significantly resistant to development of oste onecrosis accompanying infectious myelitis.
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Methotrexate inhibits osteoclastogenesis by decreasing RANKL‑induced calcium influx into osteoclast progenitors
Hiroya Kanagawa,Ritsuko Masuyama,Mayu Morita,Yuiko Sato,Yasuo Niki,Tami Kobayashi,Eri Katsuyama,Atsuhiro Fujie,Wu Hao,Toshimi Tando,Ryuichi Watanabe,Kana Miyamoto,Hideo Morioka,Morio Matsumoto,Yoshiaki Toyama,Hideyuki Saya,Takeshi Miyamoto +16 more
TL;DR: Osteoclast formation and expression of osteoclastic genes such as NFATc1 and DC-STAMP, which are induced by the cytokine RANKL, are significantly inhibited by methotrexate (MTX), and it was found that RankL-dependent calcium (Ca) influx into osteoclast progenitors was significantly inhibition by MTX.
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