Association of lncRNA SH3PXD2A-AS1 with preeclampsia and its function in invasion and migration of placental trophoblast cells

Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from...

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Vydané v:Cell death & disease Ročník 11; číslo 7; s. 583
Hlavní autori: Chen, Qian, Jiang, Sijia, Liu, Haihua, Gao, Yue, Yang, Xiaoxue, Ren, Zhonglu, Gao, Yunfei, Xiao, Lu, Hu, Haoyue, Yu, Yanhong, Yang, Xinping, Zhong, Mei
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London Nature Publishing Group UK 27.07.2020
Springer Nature B.V
Predmet:
631/136/1425
631/337/384
Adult
Age
Antibodies
Biochemistry
Biomedical and Life Sciences
Blood pressure
CCCTC-Binding Factor - metabolism
CCR7 protein
Cell Biology
Cell Culture
Cell Cycle Checkpoints - genetics
Cell Death - genetics
Cell Line
Cell migration
Cell Movement - genetics
Cell Proliferation - genetics
Correlation analysis
Female
Gene expression
Genes
Humans
Hypertension
Immunology
Life Sciences
Molecular modelling
Non-coding RNA
Pathogenesis
Placenta
Placenta - pathology
Pre-eclampsia
Pre-Eclampsia - genetics
Pre-Eclampsia - pathology
Preeclampsia
Pregnancy
Promoter Regions, Genetic - genetics
Protein Binding
Proteins
Receptors, CCR7 - metabolism
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Subcellular Fractions - metabolism
Transcription
Transcription, Genetic
Transcriptomes
Trophoblasts - metabolism
Trophoblasts - pathology
Up-Regulation - genetics
Uterus
Veins & arteries
ISSN:2041-4889, 2041-4889
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Abstract Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from preeclamptic patients and normal subjects, and identified about four hundred long non-coding RNAs differentially expressed in placentae of patients with early-onset severe preeclampsia. Here, we report our identification of lncRNA SH3PXD2A-AS1 as a potential causal factor for this disease and its downstream pathways involved in placentation. We found that expression level of SH3PXD2A-AS1 in the placentae is positively correlated with clinical severity of the patients. We demonstrated that SH3PXD2A-AS1 inhibited invasion and migration through recruiting CCCTC-binding factor (CTCF) to the promoters of SH3PXD2A and CCR7 to inhibit their transcription. Therefore, we conclude that the upregulation of lncRNA SH3PXD2A-AS1 may contribute to the pathogenesis of preeclampsia through prohibiting trophoblast invasion during placentation.
AbstractList Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from preeclamptic patients and normal subjects, and identified about four hundred long non-coding RNAs differentially expressed in placentae of patients with early-onset severe preeclampsia. Here, we report our identification of lncRNA SH3PXD2A-AS1 as a potential causal factor for this disease and its downstream pathways involved in placentation. We found that expression level of SH3PXD2A-AS1 in the placentae is positively correlated with clinical severity of the patients. We demonstrated that SH3PXD2A-AS1 inhibited invasion and migration through recruiting CCCTC-binding factor (CTCF) to the promoters of SH3PXD2A and CCR7 to inhibit their transcription. Therefore, we conclude that the upregulation of lncRNA SH3PXD2A-AS1 may contribute to the pathogenesis of preeclampsia through prohibiting trophoblast invasion during placentation.
Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from preeclamptic patients and normal subjects, and identified about four hundred long non-coding RNAs differentially expressed in placentae of patients with early-onset severe preeclampsia. Here, we report our identification of lncRNA SH3PXD2A-AS1 as a potential causal factor for this disease and its downstream pathways involved in placentation. We found that expression level of SH3PXD2A-AS1 in the placentae is positively correlated with clinical severity of the patients. We demonstrated that SH3PXD2A-AS1 inhibited invasion and migration through recruiting CCCTC-binding factor (CTCF) to the promoters of SH3PXD2A and CCR7 to inhibit their transcription. Therefore, we conclude that the upregulation of lncRNA SH3PXD2A-AS1 may contribute to the pathogenesis of preeclampsia through prohibiting trophoblast invasion during placentation.Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from preeclamptic patients and normal subjects, and identified about four hundred long non-coding RNAs differentially expressed in placentae of patients with early-onset severe preeclampsia. Here, we report our identification of lncRNA SH3PXD2A-AS1 as a potential causal factor for this disease and its downstream pathways involved in placentation. We found that expression level of SH3PXD2A-AS1 in the placentae is positively correlated with clinical severity of the patients. We demonstrated that SH3PXD2A-AS1 inhibited invasion and migration through recruiting CCCTC-binding factor (CTCF) to the promoters of SH3PXD2A and CCR7 to inhibit their transcription. Therefore, we conclude that the upregulation of lncRNA SH3PXD2A-AS1 may contribute to the pathogenesis of preeclampsia through prohibiting trophoblast invasion during placentation.
ArticleNumber 583
Author Xiao, Lu
Yang, Xinping
Gao, Yue
Ren, Zhonglu
Hu, Haoyue
Jiang, Sijia
Yang, Xiaoxue
Liu, Haihua
Gao, Yunfei
Yu, Yanhong
Zhong, Mei
Chen, Qian
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32719429$$D View this record in MEDLINE/PubMed
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Snippet Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired...
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proquest
pubmed
crossref
springer
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 583
SubjectTerms 631/136/1425
631/337/384
Adult
Age
Antibodies
Biochemistry
Biomedical and Life Sciences
Blood pressure
CCCTC-Binding Factor - metabolism
CCR7 protein
Cell Biology
Cell Culture
Cell Cycle Checkpoints - genetics
Cell Death - genetics
Cell Line
Cell migration
Cell Movement - genetics
Cell Proliferation - genetics
Correlation analysis
Female
Gene expression
Genes
Humans
Hypertension
Immunology
Life Sciences
Molecular modelling
Non-coding RNA
Pathogenesis
Placenta
Placenta - pathology
Pre-eclampsia
Pre-Eclampsia - genetics
Pre-Eclampsia - pathology
Preeclampsia
Pregnancy
Promoter Regions, Genetic - genetics
Protein Binding
Proteins
Receptors, CCR7 - metabolism
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Subcellular Fractions - metabolism
Transcription
Transcription, Genetic
Transcriptomes
Trophoblasts - metabolism
Trophoblasts - pathology
Up-Regulation - genetics
Uterus
Veins & arteries
Title Association of lncRNA SH3PXD2A-AS1 with preeclampsia and its function in invasion and migration of placental trophoblast cells
URI https://link.springer.com/article/10.1038/s41419-020-02796-0
https://www.ncbi.nlm.nih.gov/pubmed/32719429
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Volume 11
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