Sakai Akinori
   Department   Wakamatsu Hospital of the University of Occupational and Environmental Health  Hospital President, Wakamatsu Hospital
   School of Medicine  Orthopedic Surgery, Clinical Medical Sciences
   Position  
Article types journal article
Language English
Peer review Peer reviewed
Title Systemic bone loss, impaired osteogenic activity and type I muscle fiber atrophy in mice with elastase-induced pulmonary emphysema: Establishment of a COPD-related osteoporosis mouse model.
Journal Formal name:Bone
Abbreviation:Bone
ISSN code:18732763/18732763
Domestic / ForeginForegin
Volume, Issue, Page 120,114-124頁
Author and coauthor Tsukamoto Manabu, Mori Toshiharu, Wang Ke-Yong, Okada Yasuaki, Fukuda Hokuto, Naito Keisuke, Yamanaka Yoshiaki, Sabanai Ken, Nakamura Eiichiro, Yatera Kazuhiro, Sakai Akinori
Publication date 2019/03
Summary Although it is suggested that chronic obstructive pulmonary disease (COPD) and bone are related, almost all of the pathological mechanisms of COPD-related osteoporosis remain unknown. There is a mouse model showing a deterioration of bone quality after cigarette smoke exposure; however, in smoking exposure models, various factors exist that affect bone metabolism, such as smoking and body weight loss (muscle and fat mass loss). We considered it appropriate to use an elastase-induced emphysema model to exclude factors influencing bone metabolism and to investigate the influence of pulmonary emphysema on bone metabolism. The purpose of this study was to establish a COPD/emphysema-related osteoporosis mouse model by using the elastase-induced emphysema model. The lumbar vertebrae and femurs/tibiae exhibited trabecular bone loss and impaired osteogenic activity in 24-week-old male elastase-induced emphysema model mice. In addition, the model mice showed atrophy of type I muscle fibers without atrophy of type II muscle fibers. We believe that the mice described in this experimental protocol will be accepted as a COPD/emphysema-related osteoporosis mouse model and contribute to further investigations.
DOI 10.1016/j.bone.2018.10.017
PMID 30342225