Changes in expression of L-type calcium channel subunits in skeletal muscle with aging.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25670641
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Orthopaedic surgery
• Research Institution: Shinshu University
• Principal Investigator: KATO Hiroyuki 信州大学, 学術研究院医学系, 教授 (40204490)
• Co-Investigator(Kenkyū-buntansha): UCHIYAMA Shigeharu 信州大学, 学術研究院医学系, 准教授 (10242679) ; YAMADE Mitsuhiko 信州大学, 学術研究院医学系, 教授 (10263237) ; HIGUCHI Keiichi 信州大学, 学術研究院医学系, 教授 (20173156) ; NAKADA Tsutomu 信州大学, 学術研究院医学系, 講師 (70452141)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: サルコペニア / 加齢 / L型カルシウムチャネル / 骨格筋

Outline of Final Research Achievements

L-type calcium channels (LTCC) play an essential role in excitation-contraction coupling of skeletal muscle; however, it is controversial whether expression levels of LTCC subunits change in muscle atrophy. We investigated if this is the case in sarcopenia by using young (5-month-old) and aged (26-month-old) mice, and also in a mouse model of denervation-induced muscle atrophy. Absolute and specific force of tibialis anterior (TA) muscle significantly decreased with aging and denervation. Expression of CaV1.1 subunits, main subunits of LTCC, in TA was significantly lower whereas that of auxiliary CaVβ1 subunits was significantly higher in aged than young mice. In the case of denervation-induced muscle atrophy, expression of CaV1.1 subunits was unaltered whereas expression of CaVβ1 proteins but not mRNA increased. Thus, in various types of muscle atrophy, CaVβ1 protein expression may increase through the post-translational modification and be involved in the pathological process.

Free Research Field

医歯薬学　外科系臨床医学　整形外科学