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MicroRNA‐16 is involved in the pathogenesis of pre‐eclampsia via regulation of Notch2
Author(s) -
Yuan Yuan,
Wang Xiaoying,
Sun Qiuyu,
Dai Xu,
Cai Yan
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29330
Subject(s) - trophoblast , microrna , downregulation and upregulation , biology , western blot , apoptosis , microbiology and biotechnology , pathogenesis , placenta , cancer research , gene , fetus , immunology , pregnancy , genetics
In recent years, the role of microRNAs (miRNAs) in pre‐eclampsia (PE) has been demonstrated, while the relevant mechanisms of miR‐16 in PE await to be unearthed. Thus, the aim of this study is to explore whether miR‐16 exerts its function in PE, and we assumed that miR‐16 may be implicated in the occurrence of PE by adjusting the biological functions of trophoblast cells via modulating Notch2. Placental tissues of pregnant women with normal pregnancy and PE were collected to detect the expression of miR‐16, Notch2, and Notch3. The effects of miR‐16 and Notch2 on the biological functions of BeWo and JEG‐3 cells were further determined. Expression of miR‐16 and Notch2 in trophoblast cells was detected by reverse transcription quantitative polymerase chain reaction and western blot assay. Downregulated Notch2 and upregulated miR‐16 and Notch3 were found in placental tissues of PE. There was a negative correlation between Notch2 and miR‐16 expression (r = −0.769), and a positive correlation between Notch3 and miR‐16 expression (r = 0.676; p < .05). Overexpression of miR‐16 inhibited proliferation, migration, and invasion, and facilitated the apoptosis of BeWo and JEG‐3 cells, but overexpression of Notch2 reversed this trend. Overexpression of miR‐16 inhibited Notch2 expression in BeWo and JEG‐3 cells, and Notch2 was the target gene of miR‐16. Our study highlights that overexpression of miR‐16 is involved in PE by regulating the biological functions of trophoblast cells via inhibition of Notch2. This paper provides a new idea for further study of the pathogenesis of PE.