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Research Article

The diagnostic value and regulatory mechanism of miR-200a targeting ZEB1 in pregnancy-induced hypertension

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Pages 243-251 | Received 21 Nov 2019, Accepted 14 Apr 2020, Published online: 29 Apr 2020
 

ABSTRACT

Objective

To investigate the diagnostic value and regulatory mechanism of miR-200a targeting ZEB1 in pregnancy-induced hypertension (PIH).

Methods

The expression of miR-200a and ZEB1 was detected in the placenta of PIH patients, and then the human trophoblastic cell line JEG-3 was transfected and divided into different groups: control group, NC group, ZEB1 siRNA group, miR-200a inhibitor group and miR-200a inhibitor group + ZEB1 siRNA group. After transfection, cell proliferation and migration/invasion were evaluated byMTT and Transwell assays, respectively, whereas apoptosis was assessed byflow cytometry. MiR-200a was measured by qRT-PCR, while ZEB1 was detectedby Western blotting.

Results

The expression of miR-200a was gradually increased in the placenta of patients with hypertension and mild or severe preeclampsia, while the mRNA and protein levels of ZEB1 were downregulated. A dual-luciferase reporter assay was performed to confirm the targeting relationship between miR-200a andZEB1.Compared to the control, the miR-200a inhibitor caused a strongdecrease in miR-200a andan upregulation of ZEB1, with a significant enhancement ofcell proliferation, migration and invasion and a decrease in apoptosis. However, no significant alteration was observedin the miR-200a level after administration of ZEB1 siRNA, while ZEB1 was downregulated, with significant suppression of growth.

Conclusion

MiR-200a was upregulated in PIH patients, andinhibition of miR-200a may improve disease progression, as it could facilitatetrophoblastproliferation, migration and invasionandinhibitapoptosisby targeting ZEB1.

Acknowledgments

We would like to give our appreciation to the reviewers for their comments on this article.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

The study was supported by The Project of Cangzhou Science and Technology Research and Development (No. 183302044).

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