LMO2 plays differential roles in trophoblast subtypes and is associated with preeclampsia

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 troph...

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Published inBiochemical and biophysical research communications Vol. 604; pp. 43 - 50
Main Authors Chen, Yaxin, Meng, Yingying, Yu, Yanhong, Li, Wen, Shen, Yongmei, Li, Shanshan, Chang, Ying, Sun, Wei
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 14.05.2022
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Abstract 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. [Display omitted] •Compared with normal placenta, LMO2 showed decreased expression level in both CTBs and EVTs in preeclampsia placentas.•LMO2 increased cell migration in iEVT derived HTR-8/SVneo cells via targeting to NCKAP1.•LMO2 promoted cell proliferation in CTB derived JEG-3 cells via targeting to beta-Catenin.
AbstractList 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.
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.
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. [Display omitted] •Compared with normal placenta, LMO2 showed decreased expression level in both CTBs and EVTs in preeclampsia placentas.•LMO2 increased cell migration in iEVT derived HTR-8/SVneo cells via targeting to NCKAP1.•LMO2 promoted cell proliferation in CTB derived JEG-3 cells via targeting to beta-Catenin.
Author Chen, Yaxin
Sun, Wei
Chang, Ying
Meng, Yingying
Shen, Yongmei
Yu, Yanhong
Li, Wen
Li, Shanshan
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Keywords STB
NCKAP1
EVT
Wnt pathway
LMO2
Trophoblast
iEVT
CTB
eEVT
WAVE2
WAVE complex
Hippo pathway
PE
Preeclampsia
Language English
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Snippet Preeclampsia (PE) is a common obstetric disease caused by placenta development abnormality, typically characterized as inadequate trophoblast invasion and...
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SubjectTerms Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - metabolism
Cell Line, Tumor
Cell Movement
Female
Hippo pathway
Humans
LIM Domain Proteins - genetics
LIM Domain Proteins - metabolism
LMO2
Placenta - metabolism
Placentation
pre-eclampsia
Pre-Eclampsia - metabolism
prediction
Preeclampsia
Pregnancy
Proto-Oncogene Proteins - metabolism
pseudopodia
Trophoblast
Trophoblasts - metabolism
WAVE complex
Wnt pathway
Title LMO2 plays differential roles in trophoblast subtypes and is associated with preeclampsia
URI https://dx.doi.org/10.1016/j.bbrc.2022.03.033
https://www.ncbi.nlm.nih.gov/pubmed/35286869
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https://www.proquest.com/docview/2648855251
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