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32 results on '"Zhou, Heying"'

11. Mesenchymal Bmp3b expression maintains skeletal muscle integrity and decreases in age-related sarcopenia

Author

Uezumi, Akiyoshi, Ikemoto-Uezumi, Madoka, Zhou, Heying, Kurosawa, Tamaki, Yoshimoto, Yuki, Nakatani, Masashi, Hitachi, Keisuke, Yamaguchi, Hisateru, Wakatsuki, Shuji, Araki, Toshiyuki, Morita, Mitsuhiro, Yamada, Harumoto, Toyoda, Masashi, Kanazawa, Nobuo, Nakazawa, Tatsu, Hino, Jun, Fukada, So-ichiro, and Tsuchida, Kunihiro

Subjects
Gene expression -- Health aspects, Sarcopenia -- Genetic aspects -- Development and progression -- Care and treatment, Cellular proteins -- Health aspects, Phenotype -- Health aspects, Health care industry
Abstract

Age-related sarcopenia constitutes an important health problem associated with adverse outcomes. Sarcopenia is closely associated with fat infiltration in muscle, which is attributable to interstitial mesenchymal progenitors. Mesenchymal progenitors are nonmyogenic in nature but are required for homeostatic muscle maintenance. However, the underlying mechanism of mesenchymal progenitor-dependent muscle maintenance is not clear, nor is the precise role of mesenchymal progenitors in sarcopenia. Here, we show that mice genetically engineered to specifically deplete mesenchymal progenitors exhibited phenotypes markedly similar to sarcopenia, including muscle weakness, myofiber atrophy, alterations of fiber types, and denervation at neuromuscular junctions. Through searching for genes responsible for mesenchymal progenitor-dependent muscle maintenance, we found that Bmp3b is specifically expressed in mesenchymal progenitors, whereas its expression level is significantly decreased during aging or adipogenic differentiation. The functional importance of BMP3B in maintaining myofiber mass as well as muscle-nerve interaction was demonstrated using knockout mice and cultured cells treated with BMP3B. Furthermore, the administration of recombinant BMP3B in aged mice reversed their sarcopenic phenotypes. These results reveal previously unrecognized mechanisms by which the mesenchymal progenitors ensure muscle integrity and suggest that age-related changes in mesenchymal progenitors have a considerable impact on the development of sarcopenia., Introduction Sarcopenia, the loss of skeletal muscle mass and strength, constitutes an important health problem associated with adverse outcomes such as disability, poor quality of life, and even death. A [...]

Published
2021
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20. Increased MFG‐E8 at neuromuscular junctions is an exacerbating factor for sarcopenia‐associated denervation.

Author

Ikemoto‐Uezumi, Madoka, Zhou, Heying, Kurosawa, Tamaki, Yoshimoto, Yuki, Toyoda, Masashi, Kanazawa, Nobuo, Nakazawa, Tatsu, Morita, Mitsuhiro, Tsuchida, Kunihiro, and Uezumi, Akiyoshi

Subjects
*MYONEURAL junction, *SARCOPENIA, *MILKFAT, *DENERVATION, *EPIDERMAL growth factor, *ANTIGEN presenting cells
Abstract

Sarcopenia is an important health problem associated with adverse outcomes. Although the etiology of sarcopenia remains poorly understood, factors apart from muscle fibers, including humoral factors, might be involved. Here, we used cytokine antibody arrays to identify humoral factors involved in sarcopenia and found a significant increase in levels of milk fat globule epidermal growth factor 8 (MFG‐E8) in skeletal muscle of aged mice, compared with young mice. We found that the increase in MFG‐E8 protein at arterial walls and neuromuscular junctions (NMJs) in muscles of aged mice. High levels of MFG‐E8 at NMJs and an age‐related increase in arterial MFG‐E8 have also been identified in human skeletal muscle. In NMJs, MFG‐E8 is localized on the surface of terminal Schwann cells, which are important accessory cells for the maintenance of NMJs. We found that increased MFG‐E8 at NMJs precedes age‐related denervation and is more prominent in sarcopenia‐susceptible fast‐twitch than in sarcopenia‐resistant slow‐twitch muscle. Comparison between fast and slow muscles further revealed that arterial MFG‐E8 can be uncoupled from sarcopenic phenotype. A genetic deficiency in MFG‐E8 attenuated age‐related denervation of NMJs and muscle weakness, providing evidence of a pathogenic role of increased MFG‐E8. Thus, our study revealed a mechanism by which increased MFG‐E8 at NMJs leads to age‐related NMJ degeneration and suggests that targeting MFG‐E8 could be a promising therapeutic approach to prevent sarcopenia. [ABSTRACT FROM AUTHOR]

Published
2022
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24. Reduced expression of calcitonin receptor is closely associated with age-related loss of the muscle stem cell pool

Author

Ikemoto-Uezumi, Madoka, primary, Uezumi, Akiyoshi, additional, Zhang, Lidan, additional, Zhou, Heying, additional, Hashimoto, Naohiro, additional, Okamura, Kikuo, additional, Matsui, Yasumoto, additional, Tsukazaki, Koji, additional, Hosoyama, Tohru, additional, Nakatani, Masashi, additional, Morita, Mitsuhiro, additional, Yamada, Harumoto, additional, Tsuchida, Kunihiro, additional, and Fukada, So-ichiro, additional

Published
2019
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30. Genetic risk score based on the prevalence of vertebral fracture in Japanese women with osteoporosis

Author

Zhou, Heying, primary, Mori, Seijiro, additional, Ishizaki, Tatsuro, additional, Takahashi, Atsushi, additional, Matsuda, Koichi, additional, Koretsune, Yukihiro, additional, Minami, Shiro, additional, Higashiyama, Masahiko, additional, Imai, Shinji, additional, Yoshimori, Kozo, additional, Doita, Minoru, additional, Yamada, Akira, additional, Nagayama, Satoshi, additional, Kaneko, Kazuo, additional, Asai, Satoshi, additional, Shiono, Masaki, additional, Kubo, Michiaki, additional, and Ito, Hideki, additional

Published
2016
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