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miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia

Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remain...

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Autores principales: Suo, Mingli, Sun, Yanfei, Yang, Hailan, Ji, Jing, He, Yinfang, Dong, Liyuan, Wang, Yuxian, Zhang, Yanli, Zhang, Yingan, Hao, Min
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7273907/
https://www.ncbi.nlm.nih.gov/pubmed/32342983
http://dx.doi.org/10.1042/BSR20192575
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author Suo, Mingli
Sun, Yanfei
Yang, Hailan
Ji, Jing
He, Yinfang
Dong, Liyuan
Wang, Yuxian
Zhang, Yanli
Zhang, Yingan
Hao, Min
author_facet Suo, Mingli
Sun, Yanfei
Yang, Hailan
Ji, Jing
He, Yinfang
Dong, Liyuan
Wang, Yuxian
Zhang, Yanli
Zhang, Yingan
Hao, Min
author_sort Suo, Mingli
collection PubMed
description Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE.
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spelling pubmed-72739072020-06-16 miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia Suo, Mingli Sun, Yanfei Yang, Hailan Ji, Jing He, Yinfang Dong, Liyuan Wang, Yuxian Zhang, Yanli Zhang, Yingan Hao, Min Biosci Rep Cell Cycle, Growth & Proliferation Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE. Portland Press Ltd. 2020-06-04 /pmc/articles/PMC7273907/ /pubmed/32342983 http://dx.doi.org/10.1042/BSR20192575 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Cell Cycle, Growth & Proliferation
Suo, Mingli
Sun, Yanfei
Yang, Hailan
Ji, Jing
He, Yinfang
Dong, Liyuan
Wang, Yuxian
Zhang, Yanli
Zhang, Yingan
Hao, Min
miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title_full miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title_fullStr miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title_full_unstemmed miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title_short miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia
title_sort mir-183-5p suppressed the invasion and migration of htr-8/svneo trophoblast cells partly via targeting mmp-9 in preeclampsia
topic Cell Cycle, Growth & Proliferation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7273907/
https://www.ncbi.nlm.nih.gov/pubmed/32342983
http://dx.doi.org/10.1042/BSR20192575
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