摘要
目的探讨Apelin-APJ参与动脉粥样硬化的可能机制。方法RT—PCR、Western印迹、ELISA方法检测Apelin干预后人脐静脉内皮细胞ICAM-1和VCAM-1的表达，以及抑制细胞NF—κB信号通路后Apelin诱导人脐静脉内皮细胞ICAM-1，VCAM-1表达的变化。SiRNA干预APJ表达后检测内皮细胞ICAM-1，VCAM-1及NF—κB信号的变化。结果Apelin以浓度以及时间依赖方式促进黏附分子表达。Apelin通过NF-κB信号途径促进黏附分子表达。APJ沉默取消了Apelin对黏附分子表达的促进和信号分子的激活。结论Apelin-APJ通过NF-κB信号途径促进内皮细胞黏附分子表达，后者启动炎症相关动脉粥样硬化。
Objective To explore the possible mechanism of the involvement of Apelin and its receptor （APJ） in atherosclerosis. Methods Quantitative real-time RT-PCR, Western blotting and ELISA were used to detect the expression of intercellular adhesion molecule-1 （ ICAM-1 ） and vascu- lar cell adhesion molecule-1 （VCAM-1） in human umbilical vein endothelial cells （HUVECs） treated with Apelin. The Apelin-APJ-induced expressions of ICAM-1 and VCAM-1 were determined after inhibition of the nuclear factor kappa-B （NF-κB） pathway. Additionally, the Apelin-induced expression of the adhesion molecules and Apelin-stimulated cellular signal transduction in HUVECs were examined when APJ expression was inhibited by RNA interference. Results A significant in- crease was found in the expression of ICAM-1 and VCAM-1 in HUVECs treated with Apelin. NF-κB pathway was involved in Apelin-APJ-induced activation of the adhesion molecules. Inhibition of APJ expression by RNA interference abrogated Apelin-induced expression of adhesion molecules and Apelin-stimulated cellular signal transduction in HUVECs. Conclusion The Apelin-APJ system in endothelial cells is involved in endothelial inflammation-related atherosclerosis by activating the NF- κB signaling pathways to promote the expression of adhesion molecules.
出处
《医学分子生物学杂志》
CAS
2013年第3期148-153,共6页
Journal of Medical Molecular Biology
