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流体剪切应力可诱导培养的人脐静脉内皮细胞分泌单核细胞趋化蛋白-1。

Fluid shear stress induces the secretion of monocyte chemoattractant protein-1 in cultured human umbilical vein endothelial cells.

作者信息

Yu Hongmei, Zeng Yanjun, Hu Jinlin, Li Caixia

机构信息

Biomedical Engineering Center, Beijing Polytechnic University, Beijing, 100022 China.

出版信息

Clin Hemorheol Microcirc. 2002;26(3):199-207.

Abstract

In this study we investigated the patterns of fluid shear stress on induction of monocyte chemoattractant protein-1 (MCP-1) secretion in cultured human umbilical vein endothelial cells (HUVECs). MCP-1 is a potent special chemoattractant, which recruits monocytes into the sub-endothelium. This process is one of the early events of atherosclerosis. We examined the pattern of fluid shear stress inducing the secretion of MCP-1 in cultured HUVECs from the view of biomechanics. In our experiments, HUVECs were subjected to controlled levels of shear stress (4, 10, 20 dyn/cm(2)) in a parallel plate flow chamber. MCP-1 in HUVECs of different periods was measured by an immunohistochemistry method and digital image analysis; MCP-1 in perfusion was measured by sandwich ELISA. The results demonstrated the increase of MCP-1 synthesis and secretion by shear stress was time- and force-dependent. The accumulated level of MCP-1 in HUVECs under lower shear stress (4 dyn/cm(2)) for 4-5 hrs was 3-fold compared with that for static cells. When the shear stress lasted to 6 hrs, the secretion of MCP-1 was reduced to normal levels and could not be increased even when the shear stress lasted for 12 hours. 10 dyn/cm(2) had less effect on the secretion of MCP-1 compared with 4 dyn/cm(2). This research provides data for understanding the mechanism of the contribution of hemodynamic forces to atherosclerosis.

摘要

在本研究中,我们调查了流体剪切应力对培养的人脐静脉内皮细胞(HUVECs)中单核细胞趋化蛋白-1(MCP-1)分泌诱导的模式。MCP-1是一种强效的特殊趋化因子,可将单核细胞募集到内皮下。这一过程是动脉粥样硬化的早期事件之一。我们从生物力学的角度研究了流体剪切应力诱导培养的HUVECs分泌MCP-1的模式。在我们的实验中,HUVECs在平行板流动腔中受到可控水平的剪切应力(4、10、20达因/平方厘米)。采用免疫组织化学方法和数字图像分析测定不同时期HUVECs中的MCP-1;采用夹心ELISA法测定灌注液中的MCP-1。结果表明,剪切应力对MCP-1合成和分泌的增加具有时间和力依赖性。在较低剪切应力(4达因/平方厘米)下4-5小时,HUVECs中MCP-1的累积水平是静态细胞的3倍。当剪切应力持续6小时时,MCP-1的分泌降至正常水平,即使剪切应力持续12小时也无法增加。与4达因/平方厘米相比,10达因/平方厘米对MCP-1分泌的影响较小。本研究为理解血流动力学力对动脉粥样硬化影响的机制提供了数据。

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