| Theme | Osteoporosis and urolithiasis induced by microgravity | |
|---|---|---|
| Title | Regulation of bone metabolism for skeletal loading by nitric oxide synthase | |
| Publish Date | 2005/01 | |
| Author | Akinori Sakai | Department of Orthopaedic Surgery, University of Occupational and Environmental Health |
| Author | Makoto Watanuki | Department of Orthopaedic Surgery, University of Occupational and Environmental Health |
| Author | Takeshi Sakata | Department of Orthopaedic Surgery, University of Occupational and Environmental Health |
| Author | Toshitaka Nakamura | Department of Orthopaedic Surgery, University of Occupational and Environmental Health |
| [ Summary ] | The signal pathway from sensing skeletal loading to regulating bone metabolism in bone tissue has not been fully elucidated. It has been proposed that nitric oxide (NO) is a potentially important signaling molecule in the regulation of bone metabolism in health and disease states. NO synthase (NOS) has three isoforms ; neuronal NOS (nNOS, NOS I), inducible NOS (iNOS, NOS II) and endothelial NOS (eNOS, NOS III). Physiological mechanical stress increases eNOS and decreases RANKL expression from osteoprogenitor stromal cells through the ERK 1/2 kinase pathway. NO, generated by iNOS in osteoblasts, plays a critical role in increasing osteogenic activity in response to acute increases in mechanical loading after unloading. Recently, the role of nNOS in bone metabolism has also been investigated. It may be very helpful for our understanding of various skeletal disorders to clarify the mechanism underlying NO and NOS regulation of bone metabolism after skeletal loading. | |