The Effect of Abnormal Blood Flow on Human Umbilical Vein Endothelial Cells
10.16156/j.1004-7220.2019.04.09
- VernacularTitle:异常血流动力对人脐静脉内皮细胞影响
- Author:
Yebin ZHU
1
;
Yerong ZHU
2
Author Information
1. Department of Pharmaceutical Examination, Wulanchabu Medical College
2. Department of Phytology, College of Life Sciences, Nankai University
- Publication Type:Journal Article
- Keywords:
wall shear stress;
circumferential strain;
wall pressure;
human umbilical vein endothelial cells (HUVECs);
atherosclerosis (AS)
- From:
Journal of Medical Biomechanics
2019;34(4):E393-E398
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effects of abnormal blood flow on the secretion of ET-1/NO and the expression of the mRNA and the protein of ET-1, eNOS, VCAM-1, ICAM-1 and MCP-1 in human umbilical vein endothelial cells (HUVECs), so as to explore the mechanism of atherosclerosis (AS) caused by abnormal hemodynamics. MethodsThe HUVECs were divided into stress group, wall pressure group and normal group according to the different stress. The HUVECs were cultured under the corresponding stress for 24 hours and then collected. The secretion levels of NO and ET-1 were detected by enzyme method and radioimmunoassay method. The mRNA expression levels of eNOS and ET-1 were detected by qPCR. The expression levels of the mRNA and the protein of VCAM-1, ICAM-1, MCP-1 were detected by qPCR and Western blot. Results Compared with normal group, the secretion level and the mRNA expression level of ET-1 in wall pressure group increased significantly (P<0.01), and the secretion level of NO and the mRNA expression level of eNOS in stress group also increased significantly (P<0.01), The expressions level of the mRNA and the protein of VCAM-1, ICAM-1 and MCP-1 obviously increased in stress group and wall pressure group (P<0.01). Conclusions Stress or wall pressure acting on HUVECs alone could lead to its dysfunction of the secretion and the expression of gene and protein. The mechanism of AS caused by abnormal blood flow was related to these dysfunction of HUVEC.