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Biomed Pharmacother. 2017 Oct;94:341-353. doi: 10.1016/j.biopha.2017.07.130. Epub 2017 Aug 1.

miR-144 may regulate the proliferation, migration and invasion of trophoblastic cells through targeting PTEN in preeclampsia.

Author information

1
Institute for Fetology, First Hospital of Soochow University, Suzhou 215006, China; Wuxi Maternity and Children Health Hospital Affiliated Nanjing Medical University, Wuxi 214000, China.
2
Beijing Genomics Institute-Shenzhen, Shenzhen 518083, China.
3
Wuxi Maternity and Children Health Hospital Affiliated Nanjing Medical University, Wuxi 214000, China.
4
Wuxi Maternity and Children Health Hospital Affiliated Nanjing Medical University, Wuxi 214000, China. Electronic address: lingqinghu@outlook.com.

Abstract

Previous studies indicated that microRNAs (miRNAs) were aberrantly expressed in the placentas of patients with Preeclampsia (PE); however, the underlying mechanism still requires further investigation. The aim of this study is to investigate the roles of miR-144 in preeclampsia and the related mechanism. The expression of miR-144 and PTEN in 30 placentas of patients with PE and 30 normal placentas was compared; next, HTR8/SVneo cells were transfected with miR-144 mimics and miR-144 inhibitors and cultured for 48h, and the proliferation and apoptosis, cell migration and invasion of the cells were examined; furthermore, the expression PTEN, Caspase-3 and Bcl-2 was examined; next, dual luciferase reporter assay has been performed to confirm that PTEN is a direct target of miR-144; finally, HTR-8/SVneo cells were transfected with either PTEN overexpression plasmid or PTEN RNAi to determine whether knockdown or overexpression of PTEN can mimic the effect of miR-144 We have observed that the expression of miR-144 was significantly decreased and the expression of PTEN was markedly increased in placentas of patients with PE compared with normal placentas; moreover, transfection of miR-144 mimics in trophoblastic cells induced significant increase in cell proliferation, migration, invasion, and decrease in cell apoptosis, and also affected the cell cycles; on the other hand, transfection of miR-144 inhibitors has shown the opposite effects; furthermore, transient overexpression of miR-144 induced marked decrease in the expression of PTEN, Caspase-3 and increase in expression of Bcl-2 (P<0.01), while transfection of miR-144 inhibitors showed the opposite effects; finally, PTEN has been confirmed as a direct target of miR-144; finally, transfection of PTEN overexpression plasmid or PTEN RNAi can mimic the results of miR-144 inhibitor or miR-144 mimics, respectively. In conclusion, miR-144 was down-regulated in PE, and miR-144 may play important roles in the pathogenesis of PE through targeting PTEN in trophoblastic cells. These results suggested that miR-144 has the potential to become a therapeutic target for the treatment of PE.

KEYWORDS:

Migration; PTEN; Preeclampsia; Proliferation; miR-144

PMID:
28772212
DOI:
10.1016/j.biopha.2017.07.130
[Indexed for MEDLINE]
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