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lüll Potential therapeutic targets for hypoxia-induced pulmonary artery hypertension Dong L; Li Y; Hu H; Shi L; Chen J; Wang B; Chen C; Zhu H; Li Y; Li Q; Zhang L; Chen CJ Transl Med 2014[Feb]; 12 (ä): 39BACKGROUND: Hypoxic pulmonary artery hypertension (PAH) as a severe pulmonary disease is characterized by changes of pulmonary vascular reconstruction. Mitochondrial ATP-sensitive potassium channel (mitoKATP) was considered as one of factors responsible for the proliferation of hypoxic pulmonary arterial smooth muscle cells (PASMCs), although the exact mechanisms remain unclear. METHODS: Pulmonary artery hypertension was induced in rats with or without 5-hydroxydecanoate (5-HD). The mean pulmonary artery pressure, morphologic changes, mRNA and protein expressions of voltage-gated potassium channels (Kv1.5 channel), were measured. The concentrations of monocyte chemo-attractant protein-1 (MCP-1) and transforming growth factor-beta1 (TGF-beta1) were detected. Furthermore, pulmonary arterial smooth muscle cells (PASMCs) were isolated and cultured with or without hypoxia pretreated with or without 5-HD or/and Kv1.5 inhibitor 4-aminopyridine (4-AP). Mitochondrial membrane potential (Deltapsim) and the proliferation of PASMCs were detected. RESULTS: 5-HD significantly prevented the development of PAH by blocking the mitochondrial membrane depolarization, increased the expression of voltage-gated potassium channels, and reduced pulmonary hypertension mediated by TGF-beta1 or MCP-1 signaling pathway. CONCLUSION: The MitoKATP plays an important role in the development of PAH and may be therapeutic target for the treatment of disease.|*Molecular Targeted Therapy[MESH]|Animals[MESH]|Blood Pressure/drug effects[MESH]|Cell Proliferation/drug effects[MESH]|Chemokine CCL2/metabolism[MESH]|Decanoic Acids/pharmacology/therapeutic use[MESH]|Hydroxy Acids/pharmacology/therapeutic use[MESH]|Hypertension, Pulmonary/*drug therapy/*etiology/physiopathology[MESH]|Hypoxia/*complications/physiopathology[MESH]|Kv1.5 Potassium Channel/genetics/metabolism[MESH]|Male[MESH]|Membrane Potential, Mitochondrial/drug effects[MESH]|Models, Biological[MESH]|Myocytes, Smooth Muscle/drug effects/metabolism/pathology[MESH]|Potassium Channels/metabolism[MESH]|Pulmonary Artery/drug effects/metabolism/*pathology/physiopathology[MESH]|RNA, Messenger/genetics/metabolism[MESH]|Rats[MESH]|Rats, Sprague-Dawley[MESH]|Transforming Growth Factor beta1/metabolism[MESH] |