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Updated: Sep 30, 2025

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis
Published on: November 8, 2024
LMO2 plays differential roles in trophoblast subtypes and is associated with preeclampsia
Yaxin Chen1, Yingying Meng1, Yanhong Yu1
1Laboratory of Molecular Genetics, School of Medicine, Nankai University, Tianjin, China.
Preeclampsia (PE) is a common obstetric disease caused by placenta development abnormality, typically characterized as inadequate trophoblast invasion and spiral artery remodeling. In this study, we found that LMO2 level was decreased in both cytotrophoblast (CTB) and interstitial extravillous trophoblast (iEVT) in human PE placentas, and LMO2 selectively promoted cell migration in iEVT derived HTR-8/SVneo cells whereas increased proliferation in CTB derived JEG-3 cells. In mechanism, LMO2 interacted with NCKAP1, leading to destruction of WAVE regulatory complex and increased lamellipodia formation in HTR-8/SVneo cells, whereas interacted with β-catenin and up-regulated a number of core Wnt/Hippo pathway target genes in JEG-3 cells. This study revealed the differentially functional patterns of LMO2 in different trophoblast subtypes, and suggested LMO2 as a novel target for PE prediction, prevention and treatment in clinical.
Preeclampsia (PE) is a common obstetric disease caused by placenta development abnormality, typically characterized as inadequate trophoblast invasion and spiral artery remodeling. In this study, we found that LMO2 level was decreased in both cytotrophoblast (CTB) and interstitial extravillous trophoblast (iEVT) in human PE placentas, and LMO2 selectively promoted cell migration in iEVT derived HTR-8/SVneo cells whereas increased proliferation in CTB derived JEG-3 cells. In mechanism, LMO2 interacted with NCKAP1, leading to destruction of WAVE regulatory complex and increased lamellipodia formation in HTR-8/SVneo cells, whereas interacted with β-catenin and up-regulated a number of core Wnt/Hippo pathway target genes in JEG-3 cells. This study revealed the differentially functional patterns of LMO2 in different trophoblast subtypes, and suggested LMO2 as a novel target for PE prediction, prevention and treatment in clinical.
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