@inproceedings{oai:jaxa.repo.nii.ac.jp:00013812,
 author = {粂井, 康宏 and 中村, 浩 and 森田, 定雄 and 大谷, 啓一 and 下川, 仁弥太 and Kumei, Yasuhiro and Nakamura, Hiroshi and Morita, Sadao and Oya, Keiichi and Shimokawa, Hitoyata},
 book = {宇宙利用シンポジウム　第20回　平成15年度, Space Utilization Research: Proceedings of the Twentieth Space Utilization Symposium},
 month = {Mar},
 note = {The effects of microgravity or simulated microgravity (clinorotation) on the expression of pro- and anti-apoptotic molecules in rat and human osteoblasts were investigated. Rat osteoblasts were cultured aboard space shuttle and solubilized during the mission. The mRNA levels for the inducible nitric oxide synthase (iNOS) and GTP cyclohydrolase 1 (GTPCH) in flight cultures were increased as compared to ground (1 x g) controls. Data of cellular DNA amount suggested that cell death occurred in the earlier days of the mission, however, it was recovered around the days when cells were solubilized on board. Human osteoblasts were cultured under the vector-averaged gravity condition (simulated microgravity) on clinostat rotation. Simulated microgravity increased the pro-apoptotic index (Bax/Bcl-2 ratio) together with the expression of XIAP (inhibitor of apoptosis protein), resulting in no apoptotic DNA fragmentation. In osteoblasts, iNOS is involved in the early response to mechanical strain and induction of apoptosis. GTPCH is essential for iNOS activity, but is coordinately expressed with iNOS to prevent the iNOS-induced apoptosis. Increase of the Bax/Bcl-2 ratio means mitochondrial pro-apoptotic sign. The XIAP binds to the caspase-9 and blocks further apoptotic process. Co-elevation of GTPCH and iNOS, Bax/Bcl-2 and XIAP, may indicate a self-protective features against the pro-apoptotic driving force by microgravity and simulated microgravity., 資料番号: AA0046917007},
 pages = {19--20},
 publisher = {宇宙航空研究開発機構宇宙科学研究本部, Institute of Space and Astronautical Science, Japan Aerospace Exploration Agency (JAXA/ISAS)},
 title = {微小重力による骨芽細胞のアポトーシス誘導とアポトーシス抑制に関わる分子},
 year = {2004}
}