Knockdown of Aurora kinase B alleviates high glucose-triggered trophoblast cells damage and inflammation during gestational diabetes.

IF 1.7 4区 生物学 Q3 BIOLOGY Open Life Sciences Pub Date : 2025-03-06 eCollection Date: 2025-01-01 DOI:10.1515/biol-2022-1031
Yuzhuo Ma, Yongyun Shi, Yujie Liu
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Abstract

This research investigates how Aurora kinase B (AURKB) functions in trophoblast cells when they are exposed to high levels of glucose during gestational diabetes. The findings from RT-qPCR and western blotting show that when in a high-glucose environment, AURKB expression increases in both the placenta and trophoblast cells of patients with gestational diabetes mellitus. Additionally, when AURKB is silenced in high-glucose conditions, it leads to boosted proliferation of trophoblast cells and reduced inflammation. Knockdown of AURKB inhibits the expression of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway in high glucose (HG) environment. Knockdown of AURKB may ameliorate injury and inflammatory responses in HG-exposed trophoblast cell lines in part by regulating the PI3K/AKT signaling pathway.

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下调极光激酶B可减轻妊娠糖尿病期间高糖引发的滋养细胞损伤和炎症。
本研究探讨了极光激酶B (AURKB)在妊娠糖尿病期间暴露于高水平葡萄糖的滋养细胞中的功能。RT-qPCR和western blotting结果显示,在高糖环境下,妊娠糖尿病患者胎盘和滋养细胞中AURKB的表达均增加。此外,当AURKB在高糖条件下沉默时,它会导致滋养细胞增殖增强和炎症减少。敲低AURKB可抑制高糖(HG)环境下磷酸肌苷3激酶(PI3K)/蛋白激酶B (AKT)通路的表达。敲低AURKB可能通过调节PI3K/AKT信号通路部分改善hg暴露的滋养细胞系的损伤和炎症反应。
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来源期刊
CiteScore
2.50
自引率
4.50%
发文量
131
审稿时长
43 weeks
期刊介绍: Open Life Sciences (previously Central European Journal of Biology) is a fast growing peer-reviewed journal, devoted to scholarly research in all areas of life sciences, such as molecular biology, plant science, biotechnology, cell biology, biochemistry, biophysics, microbiology and virology, ecology, differentiation and development, genetics and many others. Open Life Sciences assures top quality of published data through critical peer review and editorial involvement throughout the whole publication process. Thanks to the Open Access model of publishing, it also offers unrestricted access to published articles for all users.
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