|
多重耐药基因在睫状体上皮细胞容积调节中的作用 |
| |
陈丽新 王立伟 Tim Jacob
摘 要 目的：研究多重耐药(MDR1)基因与细胞容积调节的关系。方法：用反义寡核苷酸阻抑牛眼睫状体非色素上皮细胞MDR1基因表达，在激光共聚焦显微镜下检测MDR1基因反义寡核苷酸(MDR-anti)的导入，用反射/散射技术测量由低渗液引起的细胞容积变化。结果：阳离子脂质体促进MDR-anti导入细胞，MDR-anti导入量与剂量呈依赖性增强关系(r＝0.97，P＜0.01)。人MDR-anti使低渗液引起的细胞调节性容积减小反应延迟、缓慢，容积恢复不完全(60%)，而鼠DMR-anti没有此作用。结论：人MDR-anti抑制细胞调节性容积减小，提示MDR1基因参与细胞容积调节。
主题词 寡核苷酸类， 反义；抗药性；上皮样细胞
The role of the multiple drug resistance gene in
the volume regulation of ciliary epithelial cells
CHEN Li-Xin, WANG Li-Wei, Tim Jacob
Physiological Unit, Cardiff School of Biosciences, Cardiff University, Cardiff CF1 3US, UK
Abstract AIM:The relationship between multiple drug resistance (MDR1) gene and the volume regulation was investigated.METHODS：Antisense “knock-down” approach was used to inhibit MDR1 gene expression in bovine nonpigmented ciliary epithelial cells. The uptake of MDR1 antisense oligonucleotides (MDR-anti) was detected by a confocal microscopy. Volume changes following exposure to hypotonic solution were measured using a light reflection/scattering technique. RESULTS：The transfection reagent lipofectin facilitated the uptake of MDR-anti. The uptake of hmuan MDR-anti was directly proportional to the external concentration of antisense. There was a linear relationship between them (r=0.97, P＜0.01). The regulatory volume decrease (RVD) induced by hypotonic solution was delayed and slowed down by incubating the cells with human MDR-anti. The volume of the cells only partially recovered (60%). There was no effect of mouse MDR-anti on the volume regulation. CONCLUSION：The specific MDR-anti inhibited the RVD and this suggests that MDR1 gene be involved in the volume regulation of cells.
MeSH Oligonucleotides, antisense; Drug resistance; Epithelioid cells
细胞容积调节是细胞基本功能之一，一旦这种调节失控将导致细胞死亡。渗透性细胞肿胀会引起细胞调节性容积减少(regulatory volume decrease， RVD)，使细胞容积恢复正常。有关RVD机制目前尚不清楚，有多因素参与［1～3］。多重耐药(multiple drug resistance, [1] [2] [3] 下一页
上一个医学论文： 氧化修饰和乙酰修饰低密度脂蛋白在A型清道夫受体基因敲除小鼠的清除
下一个医学论文： 急性肺损伤大鼠肺组织 和 2受体及 2受体mRNA表达的变化
|
|
|
|
|
|
|
您现在的位置： 绿色健康网 >> 医学论文 >> 基础医学论文 >> 正文