ZHANG Qing-hua, ZHAO Ying, JIANG Zhi-xin, ZHANG Shi-jun. Effect of oxidative low density lipoprotein on placental growth factor acting on release of nitric oxide and endothelial cell adhesion molecules from human umbilical vein endothelial cellsJ. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL, 2009, 30(2): 186-188.
Citation: ZHANG Qing-hua, ZHAO Ying, JIANG Zhi-xin, ZHANG Shi-jun. Effect of oxidative low density lipoprotein on placental growth factor acting on release of nitric oxide and endothelial cell adhesion molecules from human umbilical vein endothelial cellsJ. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL, 2009, 30(2): 186-188.

Effect of oxidative low density lipoprotein on placental growth factor acting on release of nitric oxide and endothelial cell adhesion molecules from human umbilical vein endothelial cells

  • Objective: To Study the effect of oxidative low density lipoprotein(ox-LDL)on placental growth factor 1(PLGF 1)acting on release of nitric oxide(NO)and endothelial cell adhesion molecules from human umbilical vein endothelial cells(ECV 304). Methods: ECV-304(2×105)were incubated in a RPMI 1640 medium containing 2% heat-inactivated fetal bovine serum with PLGF-1(20,40,80ng/mL)in the absence or presence of ox-LDL.After the cells were cultured for 3,6,12 and 24h,the medium was collected for further use.Levels of soluble inter-cell adhesion molecule 1(sICAM-1)and soluble vascular cell adhesion molecule-1(sVCAM-1)in the supernatant were measured with an ELISA quality kit and expression of NO was analyzed according to its manufacturer’s instructions. Results: PLGF-1 induced secretion of NO and endothelial cell adhesion molecules in a dose-and time-dependent manner,while ox-LDL decreased the NO level.The expression of VCAM-1 was 5-6 folds higher than that in the control group.However,the expression of ICAM-1 was only 2-3 folds higher than that in the control group. Conclusion: Oxidative injury is an independent risk factor for atherosclerosis.PLGF-1 can induce endothelial activation and up-regulate the expression of endothelial adhesion molecules,thus further deteriorating diseases.Inflammatory reaction can be controlled by inhibiting the PLGF-1 bioactivity.
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