Zhao Wei-Xiu, Wu Zhen-Ming, Liu Wei, Lin Jian-Hua
Department of Obstetrics and Gynecology, South Campus, Ren Ji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 201112, China.
Department of Obstetrics and Gynecology, Ren Ji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China
Biol Open. 2017 Aug 15;6(8):1123-1129. doi: 10.1242/bio.025767.
Notch signaling pathways play important roles in cell fate and many diseases, including preeclampsia, the dysregulation of which may be the main cause of maternal mortality. This study aimed to investigate the roles of Notch2 and Notch3 in proliferation and invasion in trophoblast cell lines (BeWo and JAR). Small hairpin RNAs targeting Notch2/Notch3 and Notch2/Notch3-overexpression vectors were designed, constructed and transfected into BeWo and JAR cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were then used to detect Notch2 and Notch3 mRNA and protein levels, and confirm the efficiency of silence and overexpression. Flow cytometry assays were conducted to evaluate the cell cycle of the two cell lines, and transwell assays were used to detect migration and invasion. Western blot analysis was also performed to show the alteration of the cell lines' physiological activities at protein level.When Notch2 was downregulated in BeWo cells, proliferation was dramatically promoted, while migration and invasion were significantly inhibited. When Notch2 was upregulated in JAR cells, proliferation was inhibited, but migration and invasion were promoted. After overexpression of Notch3 in BeWo cells, proliferation was downregulated, but migration and invasion were both upregulated. By contrast, the silencing of Notch3 expression in JAR cells significantly enhanced proliferation, but suppressed migration and invasion. These data indicated that Notch2 and Notch3 mediate the invasion and migration of BeWo and JAR cells, and may play a potential role in early onset severe preeclampsia.
Notch信号通路在细胞命运决定及包括先兆子痫在内的多种疾病中发挥着重要作用,先兆子痫的失调可能是孕产妇死亡的主要原因。本研究旨在探讨Notch2和Notch3在滋养层细胞系(BeWo和JAR)增殖和侵袭中的作用。设计、构建了靶向Notch2/Notch3的小发夹RNA及Notch2/Notch3过表达载体,并将其转染至BeWo和JAR细胞中。随后采用定量实时聚合酶链反应(qRT-PCR)和蛋白质印迹法检测Notch2和Notch3的mRNA及蛋白质水平,并确认沉默和过表达的效率。进行流式细胞术分析以评估这两种细胞系的细胞周期,采用Transwell分析检测迁移和侵袭情况。还进行了蛋白质印迹分析以显示细胞系在蛋白质水平上生理活性的改变。当BeWo细胞中Notch2表达下调时,增殖显著促进,而迁移和侵袭明显受到抑制。当JAR细胞中Notch2表达上调时,增殖受到抑制,但迁移和侵袭得到促进。在BeWo细胞中过表达Notch3后,增殖下调,但迁移和侵袭均上调。相比之下,JAR细胞中Notch3表达的沉默显著增强了增殖,但抑制了迁移和侵袭。这些数据表明,Notch2和Notch3介导了BeWo和JAR细胞的侵袭和迁移,可能在早发型重度先兆子痫中发挥潜在作用。