Transthyretin regulates the migration and invasion of JEG-3 cells

Gong,Liyun; Zhu,Lei; Wang,Shuzhen; Zhang,Zhenyu

doi:10.3892/ol.2016.5545

Transthyretin regulates the migration and invasion of JEG-3 cells

Authors:
- Liyun Gong
- Lei Zhu
- Shuzhen Wang
- Zhenyu Zhang
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Affiliations: Department of Obstetrics and Gynecology, Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China
Published online on: December 28, 2016 https://doi.org/10.3892/ol.2016.5545
Pages: 1242-1246
Copyright: © Gong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Preeclampsia (PE) is a pregnancy-specific disorder characterized by new-onset hypertension and proteinuria that occurs after 20 weeks of gestation. It involves several organs and continues to be a leading cause of maternal and perinatal morbidity and mortality worldwide. Shallow trophoblast invasion is a common pathological feature of PE. Transthyretin (TTR) is a 56-kDa homotetrameric protein that binds thyroid hormone and retinol binding protein. Dysregulated TTR expression has been found in cases of PE. The aim of the present study was to determine the functional role of TTR in the migration and invasion of JEG-3 choriocarcinoma cells. JEG-3 cells were transfected with a plasmid construct expressing TTR (pCMV-Myc-TTR) or an empty plasmid (pCMV-Myc). Cell migration and invasion capacities were assessed by Transwell migration and invasion assays, respectively. These experiments demonstrated that TTR overexpression significantly increased the migration and invasion potential of JEG-3 cells. Matrix metalloproteinases (MMPs) are a family of zinc-containing endopeptidases capable of degrading a wide range of extracellular matrix components. Western blot analysis revealed that TTR overexpression resulted in significantly increased levels of MMP2 and MMP9 in JEG-3 cells. In conclusion, our findings suggest an important role for TTR in regulating trophoblast invasion and migration, representing a possible underlying pathological and molecular mechanisms of PE.

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