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A microfluidics assay to study invasion of human placental trophoblast cells.

ABSTRACT: Pre-eclampsia, fetal growth restriction and stillbirth are major pregnancy disorders throughout the world. The underlying pathogenesis of these diseases is defective placentation characterized by inadequate invasion of extravillous placental trophoblast cells into the uterine arteries. How trophoblast invasion is controlled remains an unanswered question but is influenced by maternal uterine immune cells called decidual natural killer cells. Here, we describe an in vitro microfluidic invasion assay to study the migration of primary human trophoblast cells. Each experiment can be performed with a small number of cells making it possible to conduct research on human samples despite the challenges of isolating primary trophoblast cells. Cells are exposed to a chemical gradient and tracked in a three-dimensional microenvironment using real-time high-resolution imaging, so that dynamic readouts on cell migration such as directionality, motility and velocity are obtained. The microfluidic system was validated using isolated trophoblast and a gradient of granulocyte-macrophage colony-stimulating factor, a cytokine produced by activated decidual natural killer cells. This microfluidic model provides detailed analysis of the dynamics of trophoblast migration compared to previous assays and can be modified in future to study in vitro how human trophoblast behaves during placentation.

SUBMITTER: Abbas Y

PROVIDER: S-EPMC5454302 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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A microfluidics assay to study invasion of human placental trophoblast cells.

Abbas Yassen Y Oefner Carolin Melati CM Polacheck William J WJ Gardner Lucy L Farrell Lydia L Sharkey Andrew A Kamm Roger R Moffett Ashley A Oyen Michelle L ML

Journal of the Royal Society, Interface 20170501 130

Pre-eclampsia, fetal growth restriction and stillbirth are major pregnancy disorders throughout the world. The underlying pathogenesis of these diseases is defective placentation characterized by inadequate invasion of extravillous placental trophoblast cells into the uterine arteries. How trophoblast invasion is controlled remains an unanswered question but is influenced by maternal uterine immune cells called decidual natural killer cells. Here, we describe an <i>in vitro</i> microfluidic inva ...[more]

PMID: 28566515

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Project description:BackgroundRecent studies have shown that the abnormal expression of long-chain non-coding RNAs (lncRNAs) can significantly affect the biological function of trophoblast cells and lead to the occurrence of preeclampsia (PE). This study explores the expression of lncRNA LINC00922 in PE and its effect on the function of placental trophoblast cells, along with the corresponding molecular mechanism, providing a theoretical basis and molecular target for understanding the occurrence, early diagnosis, and targeted therapy of PE.MethodsFluorescence quantitative PCR was used to detect the expression of LINC00922 in 30 cases of PE tissues and normal tissues. The CCK-8 assay, clone formation experiment, and flow cytometry were used to detect the effects of LINC00922 knockdown or overexpression on the proliferation, colony formation, and cell cycle of HTR-8/SVneo placental trophoblast cells. The Transwell assay was used to detect the effects of LINC00922 knockdown or overexpression on the invasion and migration of HTR 8/SVneo cells, and western blot was used to detect the expression of cell cycle-related proteins and invasion and migration-related proteins.ResultsLINC00922 was highly expressed in PE tissues. Knockdown of LINC00922 significantly inhibited the proliferation, invasion, and migration of HTR-8/SVneo cells, along with colony formation and the ability to induce cell cycle arrest in the G0/G1 phase. However, overexpression of LINC00922 had the opposite effect. Knockdown or overexpression of LINC00922 significantly affected the expression of cell cycle-related proteins cyclin-dependent kinase 2 (CDK2), G1/S-specific cyclin-D1 (Cyclin D1), p21, proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 9 (MMP-9), vimentin, and E-cadherin, but had no significant effect on the expression of matrix metallopeptidase 2 (MMP-2).ConclusionsLINC00922 was highly expressed in PE, and functional experiments showed that LINC00922 could significantly affect the proliferation and invasion abilities of placental trophoblast cells, suggesting that LINC00922 may play an important role in the occurrence, early diagnosis, and treatment of PE.

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A microfluidics assay to study invasion of human placental trophoblast cells.

Publications

A microfluidics assay to study invasion of human placental trophoblast cells.

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