偶联因子6抑制肌球蛋白轻链磷酸化增加跨内皮细胞电阻  

The effect of coupling factor 6 on transendothelial resistance via phosphorylated myosin light chain of lung micro vascular endothelial cells

作　　者：李晓鲁[1] 尤淑玲 张静 何涛[3] 徐文伟[1] 戴红艳[3] 

机构地区：[1]山东大学附属千佛山医院急救中心,济南250014 [2]山东省枣庄市王开传染病医院,滕州277500 [3]山东省青岛市市立医院心脏中心,青岛266011

出　　处：《疑难病杂志》2010年第11期817-819,共3页Chinese Journal of Difficult and Complicated Cases

基　　金：山东省优秀中青年科学家奖励基金(No.2008BS03051)

摘　　要：目的探讨偶联因子6(CF6)对人肺微血管内皮细胞(LMVEC)跨内皮细胞电阻(TER)的影响。方法体外培养LMVEC,于不同时间给予不同剂量(高剂量:10^(-6) mol/L,低剂量10^(-6) mol/L)的CF6刺激,通过细胞电阻测定仪(ECIS)及Western blot观察其对TER及相关活化信号分子的影响。结果与对照组比较,CF6刺激组细胞形态无明显改变,但TER值显著增加,随着CF6孵育时间的增加,TER值明显增加,TER(ohm)峰值出现在15h后(1.39±0.02 vs 1.00±0.02,P<0.01),增加观察时间至24h发现TER维持在高水平(1.350±0.018 vs 1.000±0.023,P<0.01)。用10^(-6)和10^(-7)mol/L的CF6孵育,TER虽剂量增加,但是组间差异无统计学意义(1.39±0.02 vs 1.37±0.01)。CF6刺激组明显抑制磷酸化肌球蛋白轻链(p-MLC)水平,但是高、低剂量组间差异无统计学意义(P>0.05)。并且和TER测定结果相似,CF6抗体能够中和CF6刺激引起的p-MLC水平降低。结论 CF6可能通过抑制细胞骨架运动调节蛋白p-MLC水平,增加TER,参与内皮细胞渗透性的调节。Objective To investigate the effect of coupling factor 6（CF6） on transendothelial resistance （TER）in human lung micro vascular endothelial cells（LMVEC）.Methods In isolated and cultured LMVECs,different dosage of CF6（10^（-6） mol/L or 10 ^（-7） mol/L） or anti CF6 were added into medium of electric cell impedance sensing（ECIS） slot or culture plates.The TER and phosphorylated myosin light chain（p-MLC） levels were observed. Results Compared with control group,TER（ohm） in CF6 treated groups were significantly increased with the peak at 15h（1.39±0.02 vs 1.00±0.02,P0.01）,and maintained the high level in 24h（1.350±0.018 vs 1.000±0.023,P0.01）,and the effects were neutralized by CF6 antibody.Further study showed CF6 inhibited the expressions of p-MLC levels without significant difference among the CF6 treated groups（P0.05）.Conclusion CF6 might induce the increase of TER in human lung endothelial cells,and could be mediated by p-MLC,which is an upstream regulated signal protein of actin.

关 键 词：偶联因子6 跨内皮细胞电阻 肌球蛋白轻链磷酸化 人肺微血管内皮细胞 

分 类 号：R363[医药卫生—病理学]