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
An Essential Role for STAT6-STAT1 Protein Signaling in Promoting Macrophage Cell-Cell Fusion
Hiroya Miyamoto,Eri Katsuyama,Yoshiteru Miyauchi,Hiroko Hoshi,Kana Miyamoto,Yuiko Sato,Tami Kobayashi,Ryotaro Iwasaki,Shigeyuki Yoshida,Tomoaki Mori,Hiroya Kanagawa,Atsuhiro Fujie,Wu Hao,Hideo Morioka,Morio Matsumoto,Yoshiaki Toyama,Takeshi Miyamoto +16 more
TL;DR: It is shown that signal transducer and activator of transcription 1 (STAT1) deficiency in macrophages enhanced cell-cell fusion and elevated DC-STAMP expression in FBGCs and the STAT6-STAT1 axis regulates OC-STamp and DC- STAMP expression and governs fusogenic mechanisms in FB GCs.
Changes in bone metabolic profile associated with pregnancy or lactation.
Takeshi Miyamoto,Kei Miyakoshi,Yuiko Sato,Yoshifumi Kasuga,Satoru Ikenoue,Kana Miyamoto,Kana Miyamoto,Kana Miyamoto,Yuji Nishiwaki,Mamoru Tanaka,Masaya Nakamura,Morio Matsumoto +11 more
TL;DR: It is concluded that bone metabolic status significantly changes over the period between pregnancy and post-partum lactation, and that low bone mineral density seen in a small subset of breastfeeding-only cases likely causes post- partum vertebral fragility fractures.
Conditional Inactivation of TACE by a Sox9 Promoter Leads to Osteoporosis and Increased Granulopoiesis via Dysregulation of IL-17 and G-CSF
Keisuke Horiuchi,Tokuhiro Kimura,Takeshi Miyamoto,Kana Miyamoto,Haruhiko Akiyama,Hironari Takaishi,Hideo Morioka,Takashi Nakamura,Yasunori Okada,Carl P. Blobel,Yoshiaki Toyama +10 more
TL;DR: Findings indicate that TACE is associated with a regulation of IL-17 and G- CSF expression in vivo, and that the dysregulation in G-CSF production is causally related to both the osteoporosis-like phenotype and the defects in the hematopoietic system.
Ibandronate concomitantly blocks immobilization-induced bone and muscle atrophy.
Ryuichi Watanabe,Nobuyuki Fujita,Satoshi Takeda,Yuiko Sato,Tami Kobayashi,Mayu Morita,Takatsugu Oike,Kana Miyamoto,Yoshihiro Matsumoto,Morio Matsumoto,Masaya Nakamura,Takeshi Miyamoto +11 more
TL;DR: It is shown that skeletal muscle is a direct target of the bisphosphonate ibandronate (IBN) and that reduced muscle volume and induction of Atrogin-1 and MuRF1, both atrogenes, are significantly inhibited by IBN administration in vivo using a mouse model of muscle atrophy.
Fbxw7 acts as a critical fail-safe against premature loss of hematopoietic stem cells and development of T-ALL
Sahoko Matsuoka,Yuichi Oike,Yuichi Oike,Ichiro Onoyama,Atsushi Iwama,Fumio Arai,Keiyo Takubo,Yoichi Mashimo,Hideyuki Oguro,Eriko Nitta,Keisuke Ito,Kana Miyamoto,Hiroki Yoshiwara,Kentaro Hosokawa,Yuka Nakamura,Yumiko Gomei,Hiroko Iwasaki,Yasuhide Hayashi,Yumi Matsuzaki,Keiko Nakayama,Yasuo Ikeda,Akira Hata,Shigeru Chiba,Keiichi I. Nakayama,Toshio Suda +24 more
TL;DR: It is demonstrated that inactivation of Fbxw7 in hematopoietic cells causes premature depletion of HSCs due to active cell cycling and p53-dependent apoptosis, and functions as a fail-safe mechanism against both premature HSC loss and leukemogenesis.