双配体受体对内皮细胞粘附因子的表达调控作用
发布时间：2018-10-04 22:21
【摘要】：目的：探索溶血磷脂酰胆碱(Lysophosphatidylcholine, LPC)和质子(H+)刺激人脐静脉内皮细胞(Human umbilical vein endothelial cell, HUVEC)上细胞质子感知受体G2A后对细胞间粘附因子1(Intercellular adhesion molecule-1, ICAM-1)、血管细胞粘附因子1(Vascular cell adhesion molecule-1, VCAM-1)表达量的影响,研究相关受体介导信号通路,并探讨动脉硬化中的作用。 方法：培养HUVEC,短发夹RNA (short hairpin RNA, shRNA)-G2A质粒转染HUVEC,并用G418筛选稳定表达细胞株。PCR检测G2A在HUVEC细胞及干扰G2A基因的HUVEC细胞中的表达。在LPC和质子作用下检测HUVEC细胞及G2A基因干扰的HUVEC细胞中钙离子浓度、ICAM-1和VCAM-1表达量；检测Gi蛋白抑制剂百日咳毒素(pertussis toxin, PTX)在此过程中的作用。 结果：获得了稳定干扰的G2A基因的HUVEC细胞。质子刺激HUVEC相比对照HUVECG2A表达量降低。LPC刺激升高HUVEC胞内Ca2+浓度,质子能降低由LPC动员的Ca2+浓度。PTX能抑制由LPC引起的Ca2+浓度上升。LPC刺激G2A干扰细胞后ICAM-1, VCAM-1表达量比刺激未干扰细胞后ICAM-1, VCAM-1表达量降低。LPC单独刺激G2A干扰细胞引起ICAM-1, VACM-1表达量下降；共同刺激G2A干扰细胞ICAM-1, VACM-1表达量无变化。 结论：质子刺激能降低HUVEC中G2A表达。G2A是在HUVEC里中ICAM-1、VCAM-1表达主要相关受体。G2A干扰的HUVEC细胞中质子拮抗LPC介导的ICAM-1、VCAM-1变化。LPC活化的G2A与Gi蛋白相偶联,继而升高胞内Ca2+浓度；质子拮抗LPC引起的Ca2+浓度上升。研究结果提示,双配体受体对动脉硬化发生中起重要的调控作用。
[Abstract]:Objective: to investigate the effects of lysophosphatidylcholine (Lysophosphatidylcholine, LPC) and proton (H) (H) on cytoplasmic adhesion factor 1 (Intercellular adhesion molecule-1, ICAM-1) and vascular cell adhesion factor 1 (Vascular cell adhesion molecule-1, (Vascular cell adhesion molecule-1,) on human umbilical vein endothelial cells (Human umbilical vein endothelial cell, HUVEC). The effect of VCAM-1 expression, To study the signal pathway mediated by related receptors and to explore the role of atherosclerosis. Methods: the expression of G2A in HUVEC cells and HUVEC cells which interfered with G2A gene was detected by G418 screening and stable expression cell line. The expression of ICAM-1 and VCAM-1 in HUVEC cells and G2A gene interfering HUVEC cells were detected by LPC and proton, and the role of Gi protein inhibitor pertussis toxin (pertussis toxin, PTX) in this process was detected. Results: stable interfering G 2A gene HUVEC cells were obtained. Proton stimulated HUVEC decreased compared with control HUVECG2A expression. LPC-stimulated increased intracellular Ca2 concentration of HUVEC. Proton could reduce the concentration of Ca2 mobilized by LPC. PTX could inhibit the increase of Ca2 concentration induced by LPC. The expression of ICAM-1, VCAM-1 in G2A interfering cells stimulated by LPC was lower than that of ICAM-1, VCAM-1 after stimulation of undisturbed cells. Co-stimulation of G 2A interfered with the expression of ICAM-1, VACM-1 in the cells. Conclusion: proton stimulation can reduce the expression of G2A. G2A in HUVEC. G2A is a major receptor. G2A interferes with the expression of G2A in HUVEC. Proton antagonizes ICAM-1,VCAM-1 changes mediated by LPC. G2A activated by LPC is coupled with Gi protein, and then increases the concentration of Ca2. Proton antagonizes the increase of Ca2 concentration induced by LPC. The results suggest that double ligand receptors play an important role in the pathogenesis of atherosclerosis.
【学位授予单位】：内蒙古大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R363
[Abstract]:Objective: to investigate the effects of lysophosphatidylcholine (Lysophosphatidylcholine, LPC) and proton (H) (H) on cytoplasmic adhesion factor 1 (Intercellular adhesion molecule-1, ICAM-1) and vascular cell adhesion factor 1 (Vascular cell adhesion molecule-1, (Vascular cell adhesion molecule-1,) on human umbilical vein endothelial cells (Human umbilical vein endothelial cell, HUVEC). The effect of VCAM-1 expression, To study the signal pathway mediated by related receptors and to explore the role of atherosclerosis. Methods: the expression of G2A in HUVEC cells and HUVEC cells which interfered with G2A gene was detected by G418 screening and stable expression cell line. The expression of ICAM-1 and VCAM-1 in HUVEC cells and G2A gene interfering HUVEC cells were detected by LPC and proton, and the role of Gi protein inhibitor pertussis toxin (pertussis toxin, PTX) in this process was detected. Results: stable interfering G 2A gene HUVEC cells were obtained. Proton stimulated HUVEC decreased compared with control HUVECG2A expression. LPC-stimulated increased intracellular Ca2 concentration of HUVEC. Proton could reduce the concentration of Ca2 mobilized by LPC. PTX could inhibit the increase of Ca2 concentration induced by LPC. The expression of ICAM-1, VCAM-1 in G2A interfering cells stimulated by LPC was lower than that of ICAM-1, VCAM-1 after stimulation of undisturbed cells. Co-stimulation of G 2A interfered with the expression of ICAM-1, VACM-1 in the cells. Conclusion: proton stimulation can reduce the expression of G2A. G2A in HUVEC. G2A is a major receptor. G2A interferes with the expression of G2A in HUVEC. Proton antagonizes ICAM-1,VCAM-1 changes mediated by LPC. G2A activated by LPC is coupled with Gi protein, and then increases the concentration of Ca2. Proton antagonizes the increase of Ca2 concentration induced by LPC. The results suggest that double ligand receptors play an important role in the pathogenesis of atherosclerosis.
【学位授予单位】：内蒙古大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R363
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1 程慧娴;徐苗苗;高玮;惠康丽;金孝\，
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