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

Lu Ci

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Abstract

Objective To study the role of ERK1/2(extracellular signal-regulated kinase 1 and 2,ERK1/2 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 stages of exposure(24,48 and 72hr) on proliferation of arotic vascular smooth muscle cells of 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 ERK1/2 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 ERK1/2 may play the key role in the proliferation of VSMCs induced by Ox-LDL.

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Objective To study the role of ERK1/2(extracellular signal-regulated kinase 1 and 2,ERK1/2 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 stages of exposure(24,48 and 72hr) on proliferation of arotic vascular smooth muscle cells of 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 ERK1/2 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 ERK1/2 may play the key role in the proliferation of VSMCs induced by Ox-LDL.

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Available abstract

Objective To study the role of ERK1/2(extracellular signal-regulated kinase 1 and 2,ERK1/2 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 stages of exposure(24,48 and 72hr) on proliferation of arotic vascular smooth muscle cells of 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 ERK1/2 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 ERK1/2 may play the key role in the proliferation of VSMCs induced by Ox-LDL.

Key concepts: Vascular smooth muscle, Cell growth, Smooth muscle, Low-density lipoprotein, Chemistry, Kinase, Extracellular, Cell

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