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葡萄糖转运蛋白 1 失调通过损害滋养层细胞的功能导致子痫前期的发病。

Dysregulated GLUT1 results in the pathogenesis of preeclampsia by impairing the function of trophoblast cells.

机构信息

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian, 116044, Liaoning Province, China.

Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, 116044, China.

出版信息

Sci Rep. 2024 Oct 10;14(1):23761. doi: 10.1038/s41598-024-74489-z.

DOI:10.1038/s41598-024-74489-z
PMID:39390043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11467397/
Abstract

Preeclampsia (PE) is a common placental-origin complication of pregnancy and a major cause of morbidity and mortality among pregnant women and fetuses. However, its pathogenesis has not been elucidated. Effective strategies for prevention, screening, and treatment are still lacking. Studies have indicated that dysfunction of placental trophoblast cells, such as impaired syncytialization, proliferation, and epithelial-mesenchymal transition processes, plays a crucial role in the development of PE. Glucose transporter 1 (GLUT1) is a key protein regulating glucose transport in placental tissues. However, the effect of GLUT1 on the function of trophoblast cells in PE is not well understood. In this study, we found that GLUT1 expression is reduced in PE placental tissues. GLUT1 promotes the syncytialization process by increasing the glucose uptake ability of BeWo cells. Additionally, GLUT1 promotes the proliferation, migration, and invasion capabilities of HTR-8/SVneo cells by regulating MAPK and PI3K/AKT signaling pathways. Overall, these findings provide a new insight into understanding the biological functions of GLUT1, clarifying the pathogenesis of PE, and identifying diagnostic and therapeutic targets for PE.

摘要

子痫前期(PE)是一种常见的胎盘源性妊娠并发症,是导致孕妇和胎儿发病率和死亡率的主要原因。然而,其发病机制尚未阐明。有效的预防、筛查和治疗策略仍然缺乏。研究表明,胎盘滋养层细胞功能障碍,如合胞体化、增殖和上皮-间充质转化过程受损,在 PE 的发展中起着关键作用。葡萄糖转运蛋白 1(GLUT1)是调节胎盘组织葡萄糖转运的关键蛋白。然而,GLUT1 对 PE 滋养层细胞功能的影响尚不清楚。在本研究中,我们发现 GLUT1 在 PE 胎盘组织中的表达减少。GLUT1 通过增加 BeWo 细胞的葡萄糖摄取能力来促进合胞体化过程。此外,GLUT1 通过调节 MAPK 和 PI3K/AKT 信号通路促进 HTR-8/SVneo 细胞的增殖、迁移和侵袭能力。总之,这些发现为理解 GLUT1 的生物学功能提供了新的视角,阐明了 PE 的发病机制,并为 PE 确定了诊断和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/f729f2348216/41598_2024_74489_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/7b1116f29aea/41598_2024_74489_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/f729f2348216/41598_2024_74489_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/c97c130829ce/41598_2024_74489_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/54940d69693d/41598_2024_74489_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/6ed2654802dd/41598_2024_74489_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/6d3e15cb77b0/41598_2024_74489_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/1750f825cb45/41598_2024_74489_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/7b1116f29aea/41598_2024_74489_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e434/11467397/f729f2348216/41598_2024_74489_Fig8_HTML.jpg

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本文引用的文献

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Impact of Metabolic Stress on BeWo Syncytiotrophoblast Function.代谢应激对 BeWo 合体滋养层功能的影响。
Chembiochem. 2023 Dec 14;24(24):e202300410. doi: 10.1002/cbic.202300410. Epub 2023 Oct 24.
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HOXB3 promotes trophoblast cell proliferation, invasion, and migration to alleviate preeclampsia via mediating the Notch/Wnt/β-catenin pathway.HOXB3 通过调控 Notch/Wnt/β-连环蛋白通路促进滋养细胞增殖、侵袭和迁移,从而减轻子痫前期。
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Altered expression of nutrient transporters in syncytiotrophoblast membranes in preeclampsia placentae.
子痫前期胎盘合体滋养层细胞膜中营养转运体的表达改变。
Placenta. 2023 Aug;139:181-189. doi: 10.1016/j.placenta.2023.07.001. Epub 2023 Jul 4.
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Apelin-36 alleviates LPS-induced trophoblast cell injury by inhibiting GRP78/ASK1/JNK signaling.Apelin-36 通过抑制 GRP78/ASK1/JNK 信号通路减轻 LPS 诱导的滋养层细胞损伤。
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Fetomaternal Expression of Glucose Transporters (GLUTs)-Biochemical, Cellular and Clinical Aspects.胎儿-母体葡萄糖转运蛋白(GLUTs)的表达——生化、细胞和临床方面。
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Leveraging Optimized Transcriptomic and Personalized Stem Cell Technologies to Better Understand Syncytialization Defects in Preeclampsia.利用优化的转录组学和个性化干细胞技术更好地理解子痫前期中的合体化缺陷。
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LncRNA GAL promotes colorectal cancer liver metastasis through stabilizing GLUT1.长链非编码RNA GAL通过稳定葡萄糖转运蛋白1促进结直肠癌肝转移。
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