缺氧诱导的GST1通过抑制活性氧(ROS)积累对滋养细胞具有保护作用

Lingjuan Chen, Gaoli Chen, Lixuan Guo, Yaping Wang, Chengjin Ai
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摘要

缺氧条件是滋养层生物功能改变的典型外在因素,包括细胞增殖、迁移和侵袭。缺氧诱导的活性氧(ROS)积累导致慢性滋养层损伤并导致先兆子痫(PE)。谷胱甘肽-S-转移酶P(GSTP1)是ROS的主要调节因子。然而,GSTP1是否参与低氧条件下ROS的调节仍然是未知的。在这里,我们研究了GSTP1在妊娠早期绒毛胎盘和足月胎盘中的表达水平,以及缺氧条件对GSTP1的影响。GSTP1在妊娠早期绒毛胎盘中的表达远高于足月胎盘。缺氧暴露后,GSTP1在滋养层样细胞系JEG3细胞中显著上调。缺氧诱导的GSTP1可能通过促进GST活性来清除缺氧暴露积累的ROS。GSTP1过表达明显逆转了缺氧对缺氧诱导的细胞增殖、迁移和侵袭的抑制作用。GSTP1过表达也逆转了缺氧诱导的细胞凋亡,表明GSTP1对ROS诱导的细胞损伤具有保护作用。此外,过表达的GSTP1显著促进JEG3细胞中的细胞增殖、迁移、侵袭和集落形成能力,表明GSP1在常氧条件下也发挥促进作用。这些数据表明,缺氧诱导的GSTP1表达促进滋养层细胞的增殖、迁移和侵袭,并在缺氧条件下发挥保护作用,这可能在PE增加过程中发挥重要作用。
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Hypoxia-Induced GST1 Exerts Protective Effects on Trophoblasts via Inhibiting Reactive Oxygen Species (ROS) Accumulation
Hypoxic conditions are a typical extrinsic factor for the modification of trophoblast biological functions, including cell proliferation, migration, and invasion. Hypoxia-induced reactive oxygen species (ROS) accumulation causes chronic trophoblast injury and contributes to preeclampsia (PE). Glutathione-S-transferase P (GSTP1) is a main regulator of ROS. However, it is still unknown whether GSTP1 is involved in ROS regulation under hypoxic conditions. Here, we investigated the expression level of GSTP1 in first-trimester villi placentas compared with full-term placentas and the effect of hypoxic conditions on GSTP1. GSTP1 expression in first-trimester villi placentas was much higher than that in full-term placentas. After hypoxia exposure, GSTP1 was significantly upregulated in JEG3 cells, a trophoblast-like cell line. Hypoxic-induced GSTP1 scavenged ROS accumulated by hypoxia exposure, potentially by promoting GST activity. The inhibitory effects of hypoxia exposure on cell proliferation, migration, and invasion induced by hypoxia exposure were obviously reversed by overexpression of GSTP1. Hypoxia-induced cell apoptosis was also reversed by GSTP1 overexpression, indicating the protective effects of GSTP1 against ROS-induced cell injury. Moreover, overexpressed GSTP1 markedly promoted the cell proliferation, migration, invasion, and colony formation abilities in JEG3 cells, demonstrating that GSP1 also exerts promoting effects under normoxic conditions. These data show that hypoxia-induced GSTP1 expression facilitates trophoblast cell proliferation, migration, and invasion and exerts protective effects under hypoxic conditions, which may play an important role during the increase in PE.
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