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
Neovascular Niche for Human Myeloma Cells in Immunodeficient Mouse Bone
Hirono Iriuchishima,Keiyo Takubo,Yoshitaka Miyakawa,Ayako Nakamura-Ishizu,Yoshiteru Miyauchi,Nobuyuki Fujita,Kana Miyamoto,Takeshi Miyamoto,Eiji Ikeda,Masahiro Kizaki,Masahiro Kizaki,Yoshihisa Nojima,Toshio Suda +12 more
TL;DR: The NOG-hMM model described here is a useful system to analyze the dynamics of MM pathophysiology, interactions of MM cells with other cellular compartments, and the utility of novel anti-MM therapies.
A missense single nucleotide polymorphism in the ALDH2 gene, rs671, is associated with hip fracture
Kenichiro Takeshima,Yuji Nishiwaki,Yasunori Suda,Yasunori Suda,Yasuo Niki,Yuiko Sato,Tami Kobayashi,Kana Miyamoto,Hisaya Uchida,Wataru Inokuchi,Takashi Tsuji,Takashi Tsuji,Atsushi Funayama,Masaya Nakamura,Morio Matsumoto,Yoshiaki Toyama,Takeshi Miyamoto,Takeshi Miyamoto +17 more
TL;DR: It is demonstrated that a missense SNP in the ALDH2 gene, rs671 (ALDH2*2), is significantly associated with hip fracture and osteoporosis, and the results provide new insight into the pathogenesis of hip fracture.
The nicotinic acetylcholine receptor α7 subunit is an essential negative regulator of bone mass
Kazuaki Mito,Yuiko Sato,Tami Kobayashi,Kana Miyamoto,Eriko Nitta,Atsushi Iwama,Morio Matsumoto,Masaya Nakamura,Kazuki Sato,Takeshi Miyamoto +9 more
TL;DR: It is shown that nAchR7−/− mice exhibit increased bone mass due to decreased osteoclast formation, accompanied by elevated osteoprotegerin/RANKL ratios in serum, and administration of nicotine to wild-type mice increased serum RANKL levels, indicating vagal nerve stimulation of macrophages via α7nAch R regulates bone mass by modulating osteocline formation.
Reactive oxygen species induce chondrocyte hypertrophy in endochondral ossification
Kozo Morita,Takeshi Miyamoto,Nobuyuki Fujita,Yoshiaki Kubota,Keisuke Ito,Keiyo Takubo,Kana Miyamoto,Ken Ninomiya,Toru Suzuki,Ryotaro Iwasaki,Mitsuru Yagi,Hironari Takaishi,Yoshiaki Toyama,Toshio Suda +13 more
TL;DR: Findings indicate that ROS levels regulate inhibition of proliferation and modulate initiation of the hypertrophic changes in chondrocytes, which is crucial for the longitudinal growth and development of long bones.
Smad4 is required to inhibit osteoclastogenesis and maintain bone mass
Mayu Morita,Shigeyuki Yoshida,Ryotaro Iwasaki,Tetsuro Yasui,Yuiko Sato,Tami Kobayashi,Ryuichi Watanabe,Takatsugu Oike,Kana Miyamoto,Masamichi Takami,Keiko Ozato,Chu-Xia Deng,Hiroyuki Aburatani,Sakae Tanaka,Akihiko Yoshimura,Yoshiaki Toyama,Morio Matsumoto,Masaya Nakamura,Hiromasa Kawana,Taneaki Nakagawa,Takeshi Miyamoto +20 more
TL;DR: It is shown that TGFβs inhibit osteoclastogenesis and maintain bone-mass through Smad4 activity in osteoclasts and latent-TGFβ1-Fc could serve as a promising new therapeutic agent in bone diseases marked by excessive resorption.