Effect of dengue virus infection on expression of vascular cell adhesion molecule-1 in human vascular endothelial cells
10.3724/SP.J.1008.2008.00750
- Author:
Rui XIAO
1
Author Information
1. Clinical Skill Center
- Publication Type:Journal Article
- Keywords:
Dengue virus;
Human umbilical vein endothelial cells;
Vascular cell adhesion molecule-1
- From:
Academic Journal of Second Military Medical University
2010;29(7):750-755
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of Dengue virus 2 (DV2) on the expression and secretion of vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were primarily isolated, purified and cultured. Cells of 2-3 generations were infected with DV2 with different MOI values (1, 2, 4, 8 and 16). HUVECs cultured with RPM11640 medium were taken as negative control. The viability of HUVECs was assessed by CCK-8 assay before and at different time points after DV2 infection(6 h, 12 h, 24 h, 48 h, 72 h and 96 h). Flow cytometry was used to detect the VCAM-1 expression in HUVECs. The expression of cytoplasmic VCAM-1 mRNA was assayed by reverse transcription-polymerase chain reaction (RT-PCR). Results: When the MOI value was 2, DV2 had no significant influence on cell viability compared with the control group. DV2 infection significantly promoted the transcription of VCAM-1 mRNA compared with the control group(P<0.05). The expression of VCAM-1 mRNA peaked at 12 h after infection and remained at a higher level within 96 h(P<0.05). The expression at 12-48 h after infection was significantly higher than that at other time points(P<0.05). HUVECs hardly had VCAM-1 mRNA expression under normal condition. The expression of VCAM-1 protein was significantly increased at 12-72 h after infection compared with the control group (P<0.05). Conclusion: DV2 can increase the expression of VCAM-1 mRNA in HUVECs, which might be one of the important mechanisms for elevated vascular permeability and plasma leakage after DV2 infection.
