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作 者:冯祥[1,2] 石书明 漆洪波[1,2] 张华[1,2]
机构地区:[1]重庆医科大学附属第一医院妇产科,重庆400016 [2]重庆医科大学中国-加拿大-新西兰联合母胎医学实验室,重庆400016
出 处:《现代妇产科进展》2015年第3期161-166,共6页Progress in Obstetrics and Gynecology
基 金:国家自然科学基金(No:81100444;No:81370732);重庆市自然科学基金资助项目(CSTC;2011BB5121);重庆市卫生局科研基金资助项目(No:2011-2-046)
摘 要:目的:探讨G-蛋白偶联受体30(GPR30)在妊娠期胎盘中的表达,以及其对人胎盘滋养细胞侵袭力的影响。方法:免疫组化法检测早孕期绒毛、正常产妇胎盘和重度子痫前期患者胎盘组织中GPR30表达。用17-β-雌二醇(17β-E2)、GPR30激动剂G1和阻滞剂G15预处理体外培养绒毛组织和人绒毛外滋养细胞株HTR8/SVneo。显微镜下观察体外绒毛组织滋养细胞生长侵袭范围,Transwell侵袭实验检测HTR8/SVneo细胞侵袭能力。免疫荧光法检测绒毛组织和HTR8/SVneo细胞中GPR30蛋白表达。Western blot法检测HTR8/SVneo细胞中GPR30和MMP-9蛋白表达。结果:GPR30在早期绒毛组织和正常末期胎盘滋养细胞上都有表达,且早孕期的表达水平高于正常末期胎盘,但在重度子痫前期胎盘上GPR30蛋白表达明显减少。E2及GPR30激动剂G1可增加滋养细胞的侵袭能力,阻滞剂G15则可下调其侵袭性;E2、G1可诱导滋养细胞GPR30蛋白表达上调,而G15则下调其表达。GPR30蛋白水平与侵袭相关蛋白MMP-9表达水平有相关性。结论:GPR30可能参与人类滋养细胞侵袭力的调节,对滋养细胞的侵袭力有正性促进作用。Objective:To characterise the expression of G-Protein Coupled Receptor 30 (GPR30) in human placenta, and to determine the role of GPR30 in trophoblast invasion. Meth- ods:Placentas from first trimester, normal term and pregnancies complicated with pre-eclampsia were used in the study. The effect of 17 ^-estradiol ( E2 ), GPR30 agonist G1 and GPR30 inhibitor G15 on invasion of first trimester villous explants and human trophoblast cell line HTR8/SVneo were determined using in vitro invasion assays. Immunofluorescence and Western blot were used to investigate the GPR30 protein expression. Results:GPR30 protein expression was significantly lower in term placentas from pregnnacies complicated by pre-eclampsia compared to placentas from first trimester and normal term pregnancies. E2 and G1 treatment significantly increased the invasiveness of trophoblast cells. In contrast, the antagonist G15 significantly decreased tropho- blast invasion. In addition, E2 and G1 treatment increased while G15 decreased GPR30 protein ex- pression. Meanwhile, the results also implied that GPR30 involves in regulating the expression of MMP-9. Conclusion: GPR30 plays a role in trophoblast invasion, the up-regulation of GPR30 pro- tein level could increase trophoblast invasion.
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