阻断MaxiK通道抑制人巨噬细胞源性泡沫细胞分化-第三军医大学学报.docVIP

曲格列酮调节人巨噬细胞 Kv1.3、Kir2.1表达及膜电位 雷新军△1，张 葳△2，林显丰3，王东琦1，袁祖贻*1,4 （西安交通大学医学院第一附属医院心内科 1. 心内科，2. 儿科， 西安 710061；3.美国印第安纳大学医学院普渡心脏病学研究所，；4. 环境与疾病相关基因教育部重点实验室， 西安 710061电压依赖性钾通道内向整流钾通道以健康人外周血单核细胞源巨噬细胞为研究对象用Real time RT-PCRWestern blot技术观察曲格列酮对巨噬细胞Kv1.3Kir2.1表达的调节作用，电压敏感染料膜电位标测技术分析其对膜电位的影响。0 μmol/L曲格列酮显著抑制巨噬细胞Kv1.3的表达，mRNA和蛋白表达下降分别超过8和6成（P0.05），而对Kir2.1的表达没有明显影响（P0.05）；同时，巨噬细胞膜电位下降了约23%（P0.05）。结论 曲格列酮分化调节Kv1.3和Kir2.1表达，human macrophages LEI Xinjun△1, ZHANG Wei△1, Lin Xianfeng3, Wang Dongqi1, Yuan Zuyi*1,4 1. Department of Cardiology; 2. Department of Pediatrics, The First Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an 710061, China; 3. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, IN 46202, USA ; 4. Research Laboratory of Ion Channelopathy of Key Laboratory of Environment and Gene-related Diseases of Ministry of Education, Xi’an Jiaotong University, Xi’an 710061, China 收稿日期：2012-05-14 Abstract: Objective To investigate the effect of troglitazone on expression of Kv1.3 and Kir2.1 channel as well as transmembrane potentials in human monocyte-derived macrophages. Methods Using the cultured human monocyte-derived macrophage as study model, the effect of troglitazone on expression of Kv1.3 and Kir2.1 channel was investigated by Real time RT-PCR and Western blot. Furthermore, its effect on membrane potentials was analyzed with the optical mapping of the membrane potential with the voltage-sensitive dyes. Results The expression of Kv1.3 channel was inhibited significantly by troglitazone(50 μmol/L), and the Kv1.3 mRNA and protein expression reduced over 8 fold and 6 fold, respectively(P0.05). However, the expression of Kir2.1 channel had no significant change(P0.05). Meanwhile, the membrane potential of macrophage decreased 23% or so (P0.05). Conclusion Troglitazone differentially regulates the expression of Kv1.3 and Kir2.1 channel in human monocyte-derived macrophages, and