Sildenafil Inhibits Human Pulmonary Artery Smooth Muscle Cell Proliferation by Decreasing Capacitative Ca^<2+> Entry

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概要

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• Ca2+ is a pivotal signal in human pulmonary artery smooth muscle cells (PASMCs) proliferation. Capacitative Ca2+ entry (CCE) via the store-operated channel (SOC), which encoded by the transient receptor potential (TRP) gene, is an important mechanism for regulating intracellular Ca2+ concentration ([Ca2+]i) in PASMCs. Sildenafil, a potent type 5 nucleotide-dependent phosphodiesterase (PDE) inhibitor, has been proposed as a therapeutic tool to treat or prevent pulmonary arterial hypertension (PAH); however, the mechanism of its antiproliferative effect on PASMCs remains unclear. This study was designed to investigate the possible antiproliferative mechanism of sildenafil on human PASMCs, namely, its effect on the Ca2+-signal pathway. Cultured normal PASMCs were treated with endothelin-1 (ET-1) or ET-1 plus sildenafil separately. Cell number and viability were determined with a hemocytometer or MTT assay. [Ca2+]i was measured by loading PASMCs with fura 2-AM. Expression of the TRPC1 gene and protein was detected by RT-PCR and Western blot, respectively. The results show that sildenafil dose-dependently inhibited the proliferation of PASMCs, the enhancement of basal [Ca2+]i level, increase of CCE, and upregulation of TRPC expression induced by ET-1. These results suggest that sildenafil potently inhibits ET-1–induced PASMCs proliferation and downregulation of CCE and TRPC expression may be responsible for its antiproliferative effect.

• 社団法人 日本薬理学会の論文
• 2008-09-20

著者

• Liu Jie

  Department Of Histology And Cell Biology Unit Of Basic Medical Science Nagasaki University Graduate

• Wang Cong

  Beijing Institute Of Respiratory Medicine Beijing Chao-yang Hospital Capital Medical University

• Wang Jun

  Department Of Electrical Electronic And Information Engineering Osaka University

• Xu Meng

  Department Of Physiology Capital Medical University

• Wang Jun

  Department Of Chemistry Faculty Of Science And Engineering Saga University

• Liu Jie

  Department Of Physiology Capital Medical University

• Shi Luping

  Department Of Physiology Capital Medical University

• ZHAO Lan

  Section on Clinical Pharmacology, Faculty of Medicine, Imperial College, Hammersmith Hospital

• WANG Yuexiu

  Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University

• WANG Chen

  Beijing Institute of Respiratory Medicine, Beijing Chao-Yang Hospital, Capital Medical University

• Zhao Lan

  Section On Clinical Pharmacology Faculty Of Medicine Imperial College Hammersmith Hospital

• Wang Yuexiu

  Beijing Institute Of Respiratory Medicine Beijing Chao-yang Hospital Capital Medical University

• Liu Jie

  Department Of Cardiology Renmin Hospital Of Wuhan University

• Wang Chen

  Beijing Chao Yang Hospital Beijing Institute Of Respiratory Medicine Capital Medical University

• Wang Jun

  Department Of Physiology Capital Medical University

• Wang Jun

  Department Of Automation And Computer-aided Engineering The Chinese University Of Hong Kong

• LIU Jie

  Department of Anatomy, The Second Military Medical University

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