Molecular biological studies on the recoverly proces from disuseatrophy

2014 Fiscal Year Final Research Report

• Project/Area Number: 24500625
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: Kansai University of Welfare Sciences
• Principal Investigator: WATANABE Masahito 関西福祉科学大学, 保健医療学部, 教授 (70084902)
• Co-Investigator(Kenkyū-buntansha): MORI Yoshiaki 関西福祉科学大学, 保健医療学部, 教授 (70268192) ; YAMAJI Junko (田代 純子) 関西福祉科学大学, 健康福祉学部, 准教授 (40340559) ; YAMAMOTO Maki 関西福祉科学大学, 保健医療学部, 教授 (60240123) ; HIROSHIMA Reiko 関西福祉科学大学, 保健医療学部, 准教授 (40404777)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ミオシン重鎖タイプI / インターロイキン-6 / 熱ショック蛋白70 / カルシニューリン

Outline of Final Research Achievements

We examined effects of IL-6 or La3+ on MHC I, HSP70, and IL-6 mRNA expression level using real-time PCR method in C2C12 skeletal muscle cells. First, we examined the effect of IL-6 on MHC I, HSP70, and IL-6 mRNA expression levels. These mRNA levels were significantly increased by the incubation with IL-6. Second, we examined the effect of La3+ on MHC I, HSP70, and IL-6 mRNA expression levels. These mRNA levels were significantly increased by the incubation with La3+. The effects of La3+ on these mRNA levels are considered as a result of calcineurin activation, because it was well known that La3+ stimulate the activity of calcineurin. La3+-induced upregulation of these mRNA levels were significantly attenuated by the application of calcineurin inhibitor, cyclosporin A. These results indicate that IL-6- and La3+/calcineurin-mediated mechanisms contribute to the upregulation of MHC I mRNA levels in C2C12 cells.

Free Research Field

解剖学