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The metabolic role of LncZBTB39-1:2 in the trophoblast mobility of preeclampsia

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posted on 2018-06-04, 09:01 authored by Yamin Liu, Ting-Li Han, Xiaofang Luo, Yuxiang Bai, Xuehai Chen, Wei Peng, XiXiong Xiong, Philip N. Baker, Chao Tong, Hongbo Qi
Preeclampsia is characterized by new onset of hypertension and proteinuria after 20 weeks' gestation and is a leading cause of maternal and neonatal morbidity and mortality. The pathogenesis of preeclampsia is often associated with aberrant trophoblast function that leads to shallow placental implantation. However, the exact underlying mechanisms remain unclear. Placental LncZBTB39-1:2 expression level was investigated in 20 healthy placentae and 20 placentae with preeclampsia using qRT-PCR, and the metabolic profile of trophoblasts overexpressing LncZBTB39-1:2 in vitro was analysed using gas chromatography-mass spectrometry (GC–MS). In this study, we found that the expression of LncZBTB39-1:2 was significantly higher in preeclamptic placentae than in healthy placentae. Our metabolomics results have shown that tricarboxylic acid cycle intermediates and metabolites related to carbohydrate metabolism were decreased with the overexpression of LncZBTB39-1:2 in HTR8/SVneo cells. These findings were validated by detecting a lower level of intracellular ATP in HTR8/Vneo cells. Furthermore, the migration of HTR8/SVneo cells was compromised when cells were transfected with a plasmid encompassing LncZBTB39-1:2 overexpression. From these results, we conclude that abnormal levels of LncZBTB39-1:2 expression might lead to aberrant conditions in HTR-8/SVneo trophoblast cells. Aberrant conditions might be associated with dysregulated trophoblast migration and subsequent failure of uterine spiral artery remodelling, a pathogenesis recognised as a contributing factor in the aetiology of preeclampsia.

Funding

This study was financed by the 111 Project (Yuwaizhuan(2016)32), China.

History

Citation

Genes and Diseases, 2018

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES

Version

  • VoR (Version of Record)

Published in

Genes and Diseases

Publisher

Elsevier

eissn

2352-3042

Acceptance date

2018-04-10

Copyright date

2018

Available date

2018-06-04

Publisher version

https://www.sciencedirect.com/science/article/pii/S2352304218300096?via=ihub

Language

en

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