Up-regulation of LncRNA NEAT1 induces apoptosis of human placental trophoblasts

Abstract

The trophoblast apoptosis induced by placental oxidative stress is a contributor to the pathological development of preeclampsia (PE), whereas the molecular mechanism remains unclear. In this study, we explored the role and mechanism of Long non-coding RNA (LncRNA) NEAT1 in trophoblasts apoptosis. In the placenta tissues of PE patients and H₂O₂-treated human trophoblast cell line HTR-8/SVneo, the expressions of LncRNA NEAT1, p53, and estrogen receptor α (ESRα) were increased whereas miR-18a-5p expression was decreased. ESRα expression was up-regulated by LncRNA NEAT1 overexpression and down-regulated by miR-18a-5p overexpression in HTR-8/SVneo cells. LncRNA NEAT1 could release ESRα expression through sponging miR-18a-5p and the transcription of LncRNA NEAT1 was promoted by p53. miR-18a-5p overexpression suppressed H₂O₂-induced cell apoptosis in HTR-8/SVneo cells, while the inhibitory effect of miR-18a-5p overexpression on cell apoptosis was abrogated by LncRNA NEAT1 overexpression. In summary, LncRNA NEAT1 transcription was induced by p53 under oxidative stress condition, the high expression of LncRNA NEAT1 subsequently increased ESRα expression by sponging miR-18a-5p, thus inducing trophoblasts apoptosis.

Keywords:

• LncRNA NEAT1
• oestrogen receptor α
• miR-18a-5p
• trophoblasts apoptosis
• preeclampsia

Ethics approval and consent to participate

Our study was approved by the Ethics Committee of the Jinhua Hospital of Zhejiang University. All pregnancies enrolled in this study signed informed consent forms.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by Zhejiang Provincial Natural Science Foundation of China (NO. LQ19H040002) and Jinhua municipal science and technology bureau project (2020-3-042).