Chuting Wang , Long Zhang , Daidi Gui , Wenjing Zou , Menglei Zhu , Yu Liu , Lei Hua , Changlian Li , Rui Ding
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引用次数: 0
Abstract
1-nitropyrene (1-NP) is a toxic component of PM2.5 that adversely affects human health, especially pregnant women; however, the mechanisms are still unclear. This study aims to explore the mechanisms by which 1-NP influences trophoblast cell behaviors. HTR8/Svneo cells were treated by different concentrations of 1-NP (0, 5, 10, 20 μM) to assess clonogenic, invasive, and migratory abilities. Western blot analysis was used to assess the expression of EMT and Wnt/β-catenin pathway proteins. 1-NP significantly inhibited HTR8/Svneo cell clonogenic ability, especially at 10 μM and 20 μM (P < 0.01). Invasiveness decreased by 68.44 % at 5 μM (P < 0.05), and migration was significantly inhibited at 10 μM and 20 μM (P < 0.05). Western blot revealed increased E-cadherin and decreased Vimentin (P < 0.01), elevated β-catenin (P < 0.05), and reduced APC (P < 0.01). In summary, 1-NP impacts trophoblast cell clonogenicity, invasion, and migration by modulating EMT and Wnt/β-catenin pathways, providing novel insights into its biological effects on trophoblast cells.
期刊介绍:
Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine.
All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.