Fibroblast Inward-Rectifier Potassium Current Upregulation in Profibrillatory Atrial Remodeling
作者： Xiao-Yan Qi , Hai Huang , Balazs Ordog , Xiaobin Luo , Patrice Naud
DOI: 10.1161/CIRCRESAHA.116.305326
关键词: Endocrinology 、 Messenger RNA 、 Atrial fibrillation 、 Internal medicine 、 Membrane potential 、 Heart failure 、 Fibroblast 、 Inward-rectifier potassium ion channel 、 Patch clamp 、 Downregulation and upregulation 、 Chemistry
摘要: Rationale:Fibroblasts are involved in cardiac arrhythmogenesis and contribute to the atrial fibrillation substrate congestive heart failure (CHF) by generating tissue fibrosis. Fibroblasts display robust ion currents, but their functional importance is poorly understood. Objective:To characterize fibroblast inward-rectifier K+ current (IK1) remodeling CHF its effects on properties. Methods Results:Freshly isolated left fibroblasts were obtained from controls dogs with (ventricular tachypacing). Patch clamp was used record resting membrane potential (RMP) IK1. RMP significantly increased (from −43.2±0.8 mV, control, −55.5±0.9 mV). upregulated IK1 (eg, at −90 mV −1.1±0.2 −2.7±0.5 pA/pF) expression of KCNJ2 mRNA (by 52%) protein 80%). Ba2+ (300 μmol/L) decreased suppressed difference between CHF. Store-operated Ca2+ entry (Fura-2-acetoxymethyl ester) fibrobl...
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