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作 者:李红[1] 王萍[2] 黄晨曦 刘灵[1] 李根霞[1] Li Hong;Wang Ping;Huang Chenxi(Dept of Obstetrics and Gynecology,The Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450002;Dept of Clinical Laboratory,The Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450002)
机构地区:[1]郑州大学第三附属医院妇产科,郑州450002 [2]郑州大学第三附属医院临床检验科,郑州450002
出 处:《安徽医科大学学报》2020年第12期1915-1920,共6页Acta Universitatis Medicinalis Anhui
基 金:国家自然科学基金(编号:81702967)。
摘 要:目的研究微小RNA-34a(miR-34a)、沉默信息调节因子1(SIRT1)在子痫前期(PE)孕妇胎盘组织的表达及miR-34a通过调节SIRT1对绒毛外滋养细胞增殖和凋亡的影响。方法收集PE孕妇(PE组)和健康孕妇(对照组)的胎盘组织各30例;设计合成miR"34a模拟物、miR-34a抑制物和SIRT1siRNA并转染HTR-8/SVeno细胞;qRT-PCR技术、Westernblot法检测胎盘组织和HTR-8/SVeno细胞miR-34a和SIRT1mRNA、蛋白的表达水平;MTS法检测各组细胞的相对增殖率;流式细胞仪检测细胞的凋亡水平。结果PE组胎盘组织中miR-34a表达升高(P<0.05),SIRT1mR-NA表达降低(P<0.05)。转染miR-34a模拟物,SIRT1的表达下降,HTR-8/SVeno细胞增殖能力下降,凋亡水平升高。转染miR-34a抑制物,SIRT1表达升高,细胞增殖能力增加,凋亡水平下降。敲除SIRT1后,细胞表现出增殖能力下降,凋亡水平升高。结论miR-34a可能通过下调SIRT1的表达,抑制滋养细胞增殖,促进滋养细胞凋亡,参与子痫前期的发生发展。Objective To investigate the expression of microRNA-34 a(miR-34 a) and silent information regulator 1(SIRT1) in the placentas of patients with pre-eclampsia and the effect of miR-34 a on the expression of SIRT1 as well as the proliferation and apoptosis in HTR-8/SVeno cells.Methods Placental tissues were collected from patients with pre-eclampsia(n=30) and normal pregnant women(n=30). MiR-34 a mimic, miR-34 a inhibitor and SIRT1 siRNA were transfected into HTR-8/SVeno cells. The expressions of miR-34 a and SIRT1 were measured by qRT-PCR and Western blot. Cell proliferation was determined by MTS assay. Apotosis was detected by flow cytometry.Results The relative expression of miR-34 a was significantly elevated and SIRT1 significantly reduced in the preeclamptic placentas. Transfection with miR-34 a mimic in HTR-8/SVeno cells decreased the expression of SIRT1 mRNA and protein. Meanwhile, the rate of proliferation significantly decreased, whereas the rate of apoptosis significantly increased. However, transfection with miR-34 a inhibitor showed the opposite results. Moreover, knockdown of SIRT1 significantly inhibited the rate of proliferation and increased the rate of apoptosis of HTR-8/SVeno cells.Conclusion MiR-34 a may participate in the development of PE by inhibiting the expression of SIRT1 and the proliferation of trophoblasts and inducing the apoptosis of trophoblasts.
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