miR-224-5p 通过靶向 PANX1 抑制滋养层细胞的铁凋亡,从而缓解小鼠子痫前期症状。

IF 3 2区 医学 Q2 DEVELOPMENTAL BIOLOGY
Ying Huang, Zhiai Bai, Shuang Sui
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引用次数: 0

摘要

子痫前期(PE)是一种妊娠期特有的高发病率和高致死率疾病,胎盘滋养细胞侵袭不足是导致子痫前期发生的关键因素。本研究探讨了microRNA(miR)-224-5p在PE中的功能和潜在机制。研究发现,在 PE 小鼠模型和 PE 细胞模型的胎盘组织样本中,miR-224-5p 的表达减少。恢复 miR-224-5p 的表达可明显抑制 ROS 水平和铁变态反应,降低妊娠小鼠的血压,提高活产率,增强滋养层细胞的增殖和侵袭能力,抑制其凋亡。总之,miR-224-5p/PANX1可通过抑制铁蜕变改善滋养细胞功能障碍,这为PE的临床治疗提供了一种潜在的新选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-224-5p alleviates preeclampsia-like mouse symptoms by targeting PANX1 to inhibit ferroptosis in trophoblast cells
Preeclampsia (PE) is a high morbidity and lethality disease specific to pregnancy, and insufficient placental trophoblast invasion acts as a crucial factor contributing to PE development. The present study investigated the function and potential mechanism of microRNA (miR)-224-5p within PE. In the study, miR-224-5p expression was reduced within placental tissue samples of the PE mouse model and PE cell model. Restoration of miR-224-5p expression markedly inhibited ROS levels and ferroptosis, lowered blood pressure in pregnant mice, increased the live birth rate, and enhanced trophoblast cell proliferation and invasion as well as suppressed their apoptosis. miR-224-5p could target and suppress PANX1, and overexpression of PANX1 could significantly advance ferroptosis and cause trophoblast dysfunction, a process that might be relieved via restoring miR-224-5p expression. In conclusion, miR-224-5p/PANX1 ameliorates trophoblast dysfunction by inhibiting ferroptosis, which provides a potential new option for clinical treatment of PE.
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来源期刊
Placenta
Placenta 医学-发育生物学
CiteScore
6.30
自引率
10.50%
发文量
391
审稿时长
78 days
期刊介绍: Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.
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