The role of voltage-dependent Ca2+ channels in phenotype change in vascular smooth muscle cells

2014 Fiscal Year Final Research Report

• Project/Area Number: 22590210
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: General physiology
• Research Institution: University of the Ryukyus
• Principal Investigator: SUNAGAWA Masanori 琉球大学, 医学部, 講師 (70325835)
• Co-Investigator(Kenkyū-buntansha): MATSUSHITA Masayuki 琉球大学, 大学院医学研究科, 教授 (30273965) ; NAKAMURA Mariko 琉球大学, 大学院医学研究科, 准教授 (40180400)
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: 形質変換 / カルシウムチャネル / 血管平滑筋細胞 / 細胞増殖

Outline of Final Research Achievements

Enhanced cell proliferation of synthetic vascular smooth muscle cells (VSMC) are due to constantly activated cell cycle progression. Entry of Ca2+ are necessary both for the progression of G1 to S phase and for the M phase. We aimed to identify Ca2+ channels, which were involved in the regulation of cell cycle. The cell proliferation of VSMC was significantly inhibited by treatment with nifedipine. Exposure of VSMC to high KCl (90 mM) also significantly inhibited the cell proliferation. When beta subunit of L-type Ca2+ channel was constitutively expressed under the control by tetracyclin, the beta subunit protein was only localized in the nucleus. Microarray analysis demonstrated that 35 genes were significantly upregulated. These results suggest that the regulation of cell proliferation of VSMC might be determined by the specific pathway of Ca2+ entry and that the beta subunit in nucleus plays an important role by regulating many genes that involves cytosolic Ca2+ homeostasis.

Free Research Field

生理学