Calcitonin Increases the Activity of ERK and Bcl-2 in Osteoclasts and Reduces SDCP-induced Osteoclasts Apoptosis

• Main Authors: Yi-Chein Huang, 黃義謙
• Other Authors: Tien-Hua Chen
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/98546731906582604054

碩士 === 國立陽明大學 === 解剖學及細胞生物學研究所 === 98 === Aim : To study what the mechanism of calcitonin reduced osteoclasts apoptosis. SDCP is the newly anti-resorption drug in recent years but it mechanism of anti-resorption is not clear. To study the mechanism of calcitonin reduced SDCP-induced osteoclasts apoptosis. Method : Take the osteoclasts from the New Zealand rabbit long bones and transdifferentiation of RAW 264.7 cell line, the osteoclasts treat with inhibitor or calcitonin or SDCP to detect apoptosis association protein and osteoclasts activity by western blot, immunoprecipitation, immunocytochemistry, TUNEL and TRAP stain. Result : Calcitonin increases the activity of ERK and Bcl-2 in osteoclasts. Calcitonin decreases SDCP-induced osteoclasts apoptosis, the cleaved caspase-3 and -9 expression level is reduced and antiapoptotic protein Bcl-2 expression level is increased. Conclusion : The ERK and Bcl-2 signaling pathway are two ofmulti-signaling pathway in calcitonin reducing osteoclasts apoptosis. The signaling pathway of calcitonin reducing SDCP-induced osteoclasts apoptosis is intrinsic apoptosis pathway including the antiapoptotic protein Bcl-2.