摘要
目的:探讨半胱氨酸丰富跨膜成骨蛋白调控因子(Crim1)对肥大乳鼠心室肌细胞瞬时外向钾电流(Ito)的调控作用.方法:将1d龄SD乳鼠心室肌细胞培养48 h后分组干预.重组腺病毒空载体(Ad-null)组给予Ad-null感染细胞32 h.重组腺病毒空载体+苯肾上腺素(Ad-null+PE)组予Ad-null感染细胞8h后,再予苯肾上腺素(PE)干预24 h.Crim1过表达重组腺病毒+苯肾上腺素(Ad-Crim1+PE)组给予携带Crim1基因的重组腺病毒感染细胞8h后,再予PE干预24 h.结晶紫染色培养细胞,ImageJ软件计算细胞表面积.全细胞膜片钳技术检测Ito,计算电流密度.结果:PE干预诱导心室肌细胞肥大,减小Ito电流密度;该效应可被过表达Crim1所抑制.结论:过表达Crim1可抑制PE诱导的心室肌细胞肥大及Ito改变.
Objective:To investigate the regulation of cysteine-rich motor neuron 1(Criml)on transient outward potassium current(Ito)in neonatal rat hypertrophic ventricular myocytes.Methods:After cultured for 24 hours,the ventricular myocytes of 1-day old Sprague-Dawley rats were divided into three groups according to different intervention.Null adenoviral vectors(Ad-null)were used to infect the cells in Ad-null group for 32 hours.The cells were infected with empty adenovirus vector for eight hours,then were stimulated with phenylephrine(PE)for 24 hours in Ad-null-PE group.The cells were infected with Criml-expressing recombinant adenovirus(Ad-Criml)for eight hours,then were stimulated with phenylephrine for 24 hours in Ad-Criml-PE group.The cell surface area was evaluated using ImageJ software.Ito was detected by whole-cell patch clamp technique and current density was calculated.Results:PE inducesd ventricular myocyte hypertrophy and reduced Ito current density,which was inhibited by overexpression of Criml.Conclusions:Overexpression of Criml inhibits PEinduced ventricular myocyte hypertrophy and Ito changes.
作者
何炯红
邓娜
杨龙
唐倩
夏桂玲
杨英
黄勇淇
赵义冬
HE Jionghong;DENG Na;YANG Long;TANG Qian;XIA Guiling;YANG Yingx;HUANG Yongqi;ZHAO Yidcmg(Department of Cardiology,Guizhou Provincial People's Hospital,Guizhou 550002;Department of Cardiology People's Hospital of Guizhou Medical University,Guizhou 550025,China)
出处
《国际心血管病杂志》
2019年第6期346-350,共5页
International Journal of Cardiovascular Disease
基金
贵州省科技计划项目(黔科合基础[2019]1205号)
贵州省科学技术厅临床研究中心项目(黔科合平台人才[(2017)5405])
