Effects of Serum Amyloid A and Lysophosphatidylcholine on Intracellular Calcium Concentration in Human Coronary Artery Smooth Muscle Cells

• Tanaka Tomofumi

  Department of Cardiovascular Medicine, The University of Tokyo

• Ikeda Kenichi

  Department of Cardiovascular Medicine, The University of Tokyo

• Yamamoto Yumiko

  Department of Cardiovascular Medicine, The University of Tokyo

• Iida Haruko

  Department of Ischemic Circulatory Physiology, The University of Tokyo

• Kikuchi Hironobu

  Department of Cardiovascular Medicine, The University of Tokyo

• Morita Toshihiro

  Department of Ischemic Circulatory Physiology, The University of Tokyo

• Yamasoba Tatsuya

  Department of Otolaryngology, The University of Tokyo

• Nagai Ryozo

  Department of Cardiovascular Medicine, The University of Tokyo

• Nakajima Toshiaki

  Department of Ischemic Circulatory Physiology, The University of Tokyo

抄録

Serum amyloid A (SAA), an acute-phase protein, and lysophosphatidylcholine (LPC), an oxidized LDL component, contribute to the physiological processes of atherosclerosis and cardiovascular disease. However, the effects of SAA/LPC on human coronary artery smooth muscle cells (hCASMCs) have not been fully investigated. Therefore, we examined the effects of SAA/LPC on Ca²⁺/Mg²⁺ mobilization and its underlying mechanisms in hCASMCs. Intracellular Ca²⁺/Mg²⁺ concentration ([Ca²⁺]_i / [Mg²⁺]_i) was measured with fura-2 AM/mag-fura-2 AM. Conventional RT-PCR analysis was also performed. Both SAA and LPC increased [Ca²⁺]_i by Ca²⁺ entry. The SAA-induced Ca²⁺ entry was inhibited by Gd³⁺, SKF96365, and 2-aminoethoxydiphenyl borate (2-APB), a nonselective transient receptor potential (TRP) channel blocker, but not nifedipine. The LPC-induced Ca²⁺ entry was blocked by Gd³⁺, but not nifedipine, SKF96365 and 2-APB. U-73122 and PTX prevented the activation of SAA-, but not LPC-induced Ca²⁺ influx. LPC, but not SAA, increased [Mg²⁺]_i as well as [Ca²⁺]_i. The RT-PCR analysis revealed the expression of TRPC1/4, TRPV1/2/4, and TRPM7/8 mRNA. These results suggest that SAA/LPC activate Ca²⁺ influx in hCASMCs; SAA activates it via PTX-sensitive G-protein, PLC and TRPC pathways, while LPC activates it independently of these pathways, where TRPM7 may be partly involved. Thus, TRP protein appears to be a target molecule of Ca²⁺ signaling in hCASMCs elicited by SAA/LPC, which may play roles in coronary muscle dysfunction under pathophysiological and inflammatory conditions such as atherosclerosis.

収録刊行物

• International Heart Journal

  International Heart Journal 52 (3), 185-193, 2011

  一般社団法人 インターナショナル・ハート・ジャーナル刊行会

キーワード

• Serum amyloid A
• Human coronary arterial smooth muscle cells
• Lysophosphatidylcholine
• Transient receptor potential
• Fura-2 AM
• GTP-binding protein
• TRPM7

詳細情報

• CRID: 1390282680201347968
• NII論文ID: 130000770919
• DOI: 10.1536/ihj.52.185
• ISSN: 13493299
• ISSN: 13492365
• Web Site: http://www.jstage.jst.go.jp/article/ihj/52/3/52_3_185/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2012103208
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可