血管紧张素Ⅱ对滋养细胞侵袭力的影响  

Effect of AngⅡ on invasion of trophoblast cells

作　　者：王美[1] 李力[1] 俞丽丽[1] 郑英如[1] 王云[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所妇产科,重庆400042

出　　处：《第三军医大学学报》2006年第11期1201-1203,共3页Journal of Third Military Medical University

摘　　要：目的研究血管紧张素Ⅱ(AngⅡ)及其受体对体外培养的滋养细胞侵袭力及细胞内局灶黏附激酶(focal ad-hesion k inase,FAK)活性的影响。方法用AngⅡ及其受体拮抗剂缬沙坦处理体外培养滋养细胞,用Transwell小室模型测定体外侵袭能力,W estern b lot法检测细胞内FAK(tyr397)的磷酸化水平,同时观察量效及时效关系。结果AngⅡ浓度为10-6mol/L时,细胞侵袭力较对照组显著性升高(P<0.01),浓度为10-5mol/L时,细胞侵袭力低于对照组(P<0.05)。10-5mol/L AngⅡ处理细胞12 h时侵袭力达高峰,而对照组于48 h时达高峰。FAK(tyr397)的磷酸化水平随血管紧张素Ⅱ浓度升高而增强,10 m in时活性最强,同时发现缬沙坦能显著阻断AngⅡ的作用。结论AngⅡ通过与受体AT1R结合,可能通过激活细胞内FAK,促进滋养细胞的侵袭力。推测过度升高的AngⅡ通过干扰滋养细胞正常的浸润机制参与子痫前期的发生、发展。Objective To study the effect of angiotensin Ⅱ （Ang Ⅱ ） and its receptor （AT1R） on the invasion and focal adhesion kinase （FAK） tyrosine phosphorylation of trophoblast ceils. Methods The human trophoblast ceils were isolated and cultured, then respectively treated with either Ang Ⅱ or Valsartan. Transwell model was used to measure the invasion. The FAK phosphorylation on tyr397 was assessed by Western blotting. Results The cell invasion was significantly increased by 10^-6mol/L Ang Ⅱ （P 〈0. 01 ）, while that by 10^-5 mol/L Ang Ⅱ was lower than control ceils （ P 〈 0.05 ）. The cell invasion peaked in 12 h by 10 ^-5 mol/L Ang Ⅱ , while that of the control ceils in 48 h. Ang Ⅱ induced a dose-dependent augmentation in FAK phosphorylation. The activity of FAK reached the maximum in 10 min by 10^-5mol/L Ang Ⅱ. Valsartan could partly block the function of Ang Ⅱ. Conclusion Ang Ⅱ can promote the invasion of trophoblast ceils by combining with AT1R and activating the FAK tyrosine phosphorylation. It suggests that excessively increased Ang Ⅱ result in pathogenesis of preeclampsia through disturbing the normally invasive mechanism of trophoblast cells.

关 键 词：血管紧张素Ⅱ 滋养细胞 局灶黏附激酶 侵袭力 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R714.245[医药卫生—基础医学]