[1]陈劲松,张波,潘从泽,等.MCP-3对人脐静脉内皮细胞表达ICAM-1、VCAM-1、TF/TFPI及其凋亡的影响[J].南方医科大学学报,2013,(01):86.
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MCP-3对人脐静脉内皮细胞表达ICAM-1、VCAM-1、TF/TFPI及其凋亡的影响()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2013年01期
页码:
86
栏目:
出版日期:
2013-01-15

文章信息/Info

Title:
Effects of monocyte chemotactic protein-3 on ICAM-1, VCAM-1, TF, and TFPI expression and apoptosis in human umbilical vein endothelial cells
作者:
陈劲松张波潘从泽任磊陈韵岱
关键词:
单核细胞趋化因子-3内皮细胞粘附分子组织因子凋亡
Keywords:
 monocyte chemotactic protein-3 endothelial cell adhesive molecule tissue factor apoptosis
摘要:
目的研究单核细胞趋化因子-3(MCP-3)对人脐静脉内皮细胞(HUVECs)表达ICAM-1、VCAM-1、TF、TFPI 及其凋亡
的影响。方法分离、培养人脐静脉内皮细胞,分别给予0~3.0 ng/ml的MCP-3进行干预,确定MCP-3对HUVECs的最适作用
浓度,以此浓度干预HUVECs,在MCP-3 加药之前1 h 分别给予MCP-3 抗体(20 ng/ml)、PI3K抑制剂LY-294002(5 mmol/ml)
处理细胞,MCP-3 作用24 h 后提取各组总RNA、总蛋白,用RT-PCR、Western blot 分别检测干预后的ICAM-1、VCAM-1、TF、
TFPI 的表达。模拟病理状态,用ox-LDL 干预HUVECs与空白组对照,24 h 后提取各组总RNA、总蛋白,用RT-PCR、Western
Blot 分别检测各组MCP-3 表达情况。最后,用MCP-3 及MCP-3+CCR2 拮抗剂RS102895(6μmol/L)分别干预HUVECs,作用
24、48 h 分别检测HUVECs凋亡率及caspase3 的表达,并与空白对照组比较。结果MCP-3 对HUVECs的最适作用浓度为
0.3 ng/ml(P<0.05);MCP-3 可诱导HUVECs 细胞中ICAM-1、VCAM-1、TF 表达的增加,同时可抑制TFPI 表达(P<0.05);
MCP-3 抗体和LY-294002 可分别拮抗、抑制此作用(P<0.05);ox-LDL 可上调HUVECs表达MCP-3(P<0.05);作用24、48 h 后
MCP-3 可明显诱导HUVECs凋亡,CCR2 抑制剂可拮抗此作用。结论ox-LDL 可诱导HUVECs表达MCP-3,MCP-3 可诱导
HUVECs凋亡,且可能部分通过PI3K信号通路影响HUVECs功能。
Abstract:
Objective To investigate the effect of monocyte chemotactic protein-3 (MCP-3) on the expressions of intercellular
adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tissue factor (TF, and tissue factor pathway
inhibitor (TFPI) and cell apoptosis in human umbilical vein endothelial cells (HUVECs). Methods Cultured HUVECs were
treated with MCP-3 at the optimal concentration determined previously 1 h after treatments with or without MCP-3 antibody
(20 ng/ml), PI3K inhibitor, or LY-294002 (5 mmol/ml). The expressions of ICAM-1, VCAM-1, TF and TFPI were analyzed using
RT-PCR and Western blot after the treatments. MCP-3 mRNA and protein expressions were detected in HUVECs exposed to
50 μg/ml ox-LDL for 24 h. The cell apoptosis and caspase-3 protein production in HUVECs treated with MCP-3 or with MCP-3
plus CCR2 antagonist for 24 h and 48 h were evaluated by flow cytometry and Western blotting. Results At the optimal
concentration of 0.3 ng/ml, MCP-3 treatment for 24 h caused significantly increased ICAM-1, VCAM-1, and TF expressions
with lowered expression of TFPI in HUVECs (P<0.05), and such effects were significantly inhibited by the application of
MCP-3 antibody, PI3K inhibitor, or LY-294002 (P<0.05). Ox-LDL exposure significantly increased the expression of MCP-3 in
HUVECs (P<0.05). HUVECs showed a significantly increased apoptosis rate after treatment with MCP-3 or with MCP-3 plus
CCR2 antagonist (P<0.05), and the apoptosis rate increased significantly as the treatment time prolonged (P<0.05); caspase-3
protein expression in the cells showed a similar pattern of alterations following the treatments. Conclusion ox-LDL can induce
MCP-3 expression in HUVECs. MCP-3 induces apoptosis of HUVECs and significantly affects the cellular function partially
through the PI3K signaling pathway.

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更新日期/Last Update: 1900-01-01