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卢次勇, 凌文华, 马静, 吴聪娥. ERK1/2在氧化型低密度脂蛋白诱导血管平滑肌细胞增殖中的作用[J]. 中国公共卫生, 2002, 18(11): 1286-1288. DOI: 10.11847/zgggws2002-18-011-03
引用本文: 卢次勇, 凌文华, 马静, 吴聪娥. ERK1/2在氧化型低密度脂蛋白诱导血管平滑肌细胞增殖中的作用[J]. 中国公共卫生, 2002, 18(11): 1286-1288. DOI: 10.11847/zgggws2002-18-011-03
LU Ci yong, LING Wen hua, MA Jing, . Role of ERK1/2 in Proliferation of Vascular Smooth Muscle Cells Induced by Oxidized Low Density Lipoprotein[J]. Chinese Journal of Public Health, 2002, 18(11): 1286-1288. DOI: 10.11847/zgggws2002-18-011-03
Citation: LU Ci yong, LING Wen hua, MA Jing, . Role of ERK1/2 in Proliferation of Vascular Smooth Muscle Cells Induced by Oxidized Low Density Lipoprotein[J]. Chinese Journal of Public Health, 2002, 18(11): 1286-1288. DOI: 10.11847/zgggws2002-18-011-03

ERK1/2在氧化型低密度脂蛋白诱导血管平滑肌细胞增殖中的作用

Role of ERK1/2 in Proliferation of Vascular Smooth Muscle Cells Induced by Oxidized Low Density Lipoprotein

  • 摘要: 目的 研究细胞外信号调节蛋白激酶(extracellular signal-regulated kinase 1 and 2,ERK1/2或p42-44MARK)信号通路在氧化型低密度脂蛋白(oxidized low density lipoprotein,Ox-LDL)诱导血管平滑肌细胞增殖中的作用.方法 采用3个时间水平(24h、48h、72h),4个剂量水平(0,50,100,200μg/ml)的两因素析因设计观察Ox-LDL对兔主动脉血管平滑肌细胞(vascular smooth musclecels,VSMCs)增殖影响的时间、剂量效应关系;Ox-LDL对兔主动脉血管平滑肌细胞ERK1/2活性影响;ERK1/2的特异断剂U0126对Ox-LDL诱导兔主动脉血管平滑肌细胞增殖的影响.结果 Ox-LDL在剂量为50,100μg/ml时,可诱导血管平滑肌细胞增殖,当Ox-LDL剂量达到200μg/ml时,细胞增殖能力迅速降低,并与其作用时间和剂量显着相关(P值均<0.01);Ox-LDL可引起血管平滑肌细胞ERK1/2活性的改变;ERK1/2的特异阻断剂U0126可完全抑制Ox-LDL诱导的VSMCs增殖.结论 Ox-LDL诱导血管平滑肌细胞增殖与其作用浓度、时间相关;ERK1/2信号通路可能在Ox-LDL诱导的血管平滑肌细胞增殖过程中起着关键的信号转导作用.

     

    Abstract: Objective To study the role of ER K1/2(extracellular signal-regulated kinase 1 and 2,ER K1/2 or p42- 44MARK)signal pathway in proliferation of vascular smooth muscle cells induced by oxidized low density lipoprotein.Methods Two-factorial experiment was designed to explore the influence of four dosage levels of Ox-LDL(0,50,100,200 μg/ml)at three different stagesof exposure(24,48 and 72hr)onproliferation of arotic vascular smooth muscle cellsof rabbit.Activities of ERK1/2 in the cultural vascular smooth muscle cells were observed with different epxosure level of Ox-LDL at different time.Special inhibitor(U0126)of ERK1/2 was used to investigate the role of ER K1/2 in proliferation of the aortic VSMCs induced by Ox-LDL.Results The proliferation of VSMCs was higher than that of control group when the cell treated with Ox-LDL at levels of 50,100μg/ml.But the proliferation of VSMCs induced by Ox-LDL was seriously reduced at 200μg/ml.The activity of ERK1/2 was also changed after the cells were treated by Ox-LDL.Special inhibitor(U0126) could inhibit cell proliferation induced by Ox-LDL.Conclusion Ox-LDL induced the proliferation of VSMCs,which were associated with the dose and time of expousre.The signal pathway of ER K1/2 may play the key role in the proliferation of VSMCs induced by Ox-LDL.

     

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