摘要
目的利用慢病毒构建人趋化因子受体1(chemokine receptor-like 1,CMKLR1)基因缺陷性小鼠血管平滑肌细胞株,观察沉默CMKLR1基因后血管平滑肌细胞的增殖情况。方法将正常血管平滑肌细胞、CMKLR1基因干扰对照血管平滑肌细胞株、CMKLR1基因缺陷性血管平滑肌细胞株分成正常组、增殖组、对照组和CMKLR1沉默组,增殖组、对照组、CMKLR1沉默组加入血小板源性生长因子-BB促进增殖,采用细胞计数和细胞增殖实验(Brdu法)检测血管平滑肌细胞增殖。结果增殖组血管平滑肌细胞的细胞数目和Brd U A值显著高于正常组(P均<0.05);与正常组相比,CMKLR1沉默组的血管平滑肌细胞数目和Brd U A值显著降低(P均<0.05);与此同时,对照组与正常组之间的血管平滑肌细胞增殖情况差异无统计学意义(P>0.05)。结论沉默CMKLR1受体可以抑制小鼠血管平滑肌细胞的增殖。
Objective To explore the proliferation property of vascular smooth muscle cells in the stable CMKLR1 gene knock - down mouse vascular smooth muscle cells （VSMCs） line. Methods The normal VSMCs, CMKLR1 gene interfering control VSMCs line, stable CMKLR1 gene knockdown VSMCs line were divided into nromal group,PDGF group, control group and CMKLR1 knockdown group, The PDGF group,control group and CMKLR1 knockdown group were given platelet- derived growth factor- BB （PDGF- BB） to initiate proliferation of VSMCs. Cell number counting and BrdU measurement were employed to investigate the proliferation property of VSMCs. Results The VSMCs number and BrdU A value of PDGF group significantly increased which was higher than those of normal group （ both P 〈 0. 05）. Compared with normal group, the CMKLR1 knockdown group obviously decreased in VSMCs number and BrdU A value （ both P 〈 0.05）. Simultaneously, there was no significant difference in the proliferation of VSMCs between normal group and control group. Conclusion Inhibiting CMKLR1 signal transduction pathway can prevent the proliferation of mouse vascular smooth muscle cells.
出处
《医学研究杂志》
2016年第4期76-79,84,共5页
Journal of Medical Research
基金
深圳市重点资助科技计划(201201022)
关键词
血管平滑肌细胞
人趋化因子受体1
信号通路
增殖
Vascular smooth muscle cell
Chemerin
Signal transduction pathway
Proliferation
