Partial least squares-based gene expression analysis in preeclampsia

Jiang, Fangping; Yang, Ying; Li, J; Li, W; Luo, Yiliao; Li, Y; Zhao, Hengyu; Wang, X; Guo, Yin; Wu, Zeyu

doi:10.4238/2015.june.18.2

Cited by 5 publications

(7 citation statements)

References 25 publications

(24 reference statements)

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“…In recent years, the role of ITGB1 in the development of PE has attracted much attention from researchers, and studies have increasingly shown that ITGB1 is involved in regulating the development of PE 10,20 . Through the analysis of differential genes in PE, ITGB1 is downregulated in the placental tissues of PE patients, 9 which is similar to the results of the present study. We found that ITGB1 expression was significantly downregulated in the placental tissues from PE patients, as compared with that of normal pregnant women.…”

Section: Discussionsupporting

confidence: 88%

“…It has been shown that ITGB1 is involved in the regulation of cell differentiation, proliferation, migration, and other biological behaviors through a unique pathway of signal transduction, 8 and has great functions in mediating cell adhesion and migration. Accumulating evidence demonstrated that ITGB1 expression is downregulated in placental tissues of PE patients, pointing to the potential effect of ITGB1 on PE 9 . Other studies indicated that the function of placental trophoblasts in PE patients could be influenced by the regulation of ITGB1 expression 10,11 .…”

Section: Introductionmentioning

confidence: 99%

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Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

Shu

Han

et al. 2021

J of Obstet and Gynaecol

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Aims Abnormal trophoblast invasion is one of the onsets of preeclampsia (PE). Studies found that integrin β1 (ITGB1) is closely related to PE, but the role of ITGB1 in the progression of trophoblast remained unclear. Therefore, we studied the functional role of ITGB1 in PE and its effects on trophoblast. Methods ITGB1 expression in placenta tissues was determined by quantitative real‐time polymerase chain reaction (qRT‐PCR). The effects of transfection on HTR‐8/SVneo cells were analyzed by qRT‐PCR and western blotting. After cell transfection, colony formation assay, flow cytometry, wound healing assay, and transwell assay were performed to detect cell proliferation, apoptosis, migration, and invasion. Western blotting assay was used for determining phosphoinositide 3 kinase (PI3K) and protein kinase B (Akt) signaling pathway. After inhibiting PI3K/Akt pathway, apoptosis‐regulated proteins were detected by western blotting, and the effects of inhibitor on the migration and invasion changes were examined. Results ITGB1 was downregulated in placenta tissues from PE patients, as compared with normal. ITGB1 overexpression in HTR‐8/SVneo cells enhanced cell proliferation, migration, and invasion, reduced cell apoptosis, and improved phosphorylation of PI3K and Akt. However, ITGB1 depletion resulted in an opposite effect to its overexpression. Inhibition of PI3K/Akt pathway completely blocked the effect of ITGB1 overexpression on cells, because we observed that apoptosis‐regulated proteins were highly upregulated, and that cell migration and invasion were reduced. Conclusion ITGB1 regulated HTR‐8/SVneo cell progression by activation of the PI3K/Akt pathway.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

Shu

Han

et al. 2021

J of Obstet and Gynaecol

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“…Two previous studies have reported that ITGB1 is related to PE through encoding the beta subunit of integrin. Additionally, up-regulated miR-29b might contribute to PE via its target genes ITGB1 and MCL1[ 35 – 36 ]. The Mtd/Mcl-1 system plays a crucial role in regulating trophoblast cell functions in both physiological and pathological conditions; Mcl-1 induces apoptosis and reduced proliferation, while Mtd likely shows different properties[ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of key microRNAs and genes in preeclampsia by bioinformatics analysis

et al. 2017

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Preeclampsia is a leading cause of perinatal maternal–foetal mortality and morbidity. The aim of this study is to identify the key microRNAs and genes in preeclampsia and uncover their potential functions. We downloaded the miRNA expression profile of GSE84260 and the gene expression profile of GSE73374 from the Gene Expression Omnibus database. Differentially expressed miRNAs and genes were identified and compared to miRNA-target information from MiRWalk 2.0, and a total of 65 differentially expressed miRNAs (DEMIs), including 32 up-regulated miRNAs and 33 down-regulated miRNAs, and 91 differentially expressed genes (DEGs), including 83 up-regulated genes and 8 down-regulated genes, were identified. The pathway enrichment analyses of the DEMIs showed that the up-regulated DEMIs were enriched in the Hippo signalling pathway and MAPK signalling pathway, and the down-regulated DEMIs were enriched in HTLV-I infection and miRNAs in cancers. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses of the DEGs were performed using Multifaceted Analysis Tool for Human Transcriptome. The up-regulated DEGs were enriched in biological processes (BPs), including the response to cAMP, response to hydrogen peroxide and cell-cell adhesion mediated by integrin; no enrichment of down-regulated DEGs was identified. KEGG analysis showed that the up-regulated DEGs were enriched in the Hippo signalling pathway and pathways in cancer. A PPI network of the DEGs was constructed by using Cytoscape software, and FOS, STAT1, MMP14, ITGB1, VCAN, DUSP1, LDHA, MCL1, MET, and ZFP36 were identified as the hub genes. The current study illustrates a characteristic microRNA profile and gene profile in preeclampsia, which may contribute to the interpretation of the progression of preeclampsia and provide novel biomarkers and therapeutic targets for preeclampsia.

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“…In placental explants during early pregnancy, hypoxia reduced the expression of SOD1 and increased cell apoptosis ( Kohan-Ghadr et al, 2019 ). Network analysis indicated that JUND and UBB are transcriptional regulators involved in PE ( Jiang et al, 2015 ; Moslehi et al, 2014 ). NFIL3 is essential for normal placental and embryonic development, while SP3 activity is required for normal embryonic development ( Krüger et al, 2007 ; Redhead et al, 2016 ).…”

Section: Resultsmentioning

confidence: 99%

Trophoblast Cell Subtypes and Dysfunction in the Placenta of Individuals with Preeclampsia Revealed by Single-Cell RNA Sequencing

Zhou

Wang

Yang

et al. 2022

Molecules and Cells

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Trophoblasts, important functional cells in the placenta, play a critical role in maintaining placental function. The heterogeneity of trophoblasts has been reported, but little is known about the trophoblast subtypes and distinctive functions during preeclampsia (PE). In this study, we aimed to gain insight into the cell type-specific transcriptomic changes by performing unbiased single-cell RNA sequencing (scRNA-seq) of placental tissue samples, including those of patients diagnosed with PE and matched healthy controls. A total of 29,006 cells were identified in 11 cell types, including trophoblasts and immune cells, and the functions of the trophoblast subtypes in the PE group and the control group were also analyzed. As an important trophoblast subtype, extravillous trophoblasts (EVTs) were further divided into 4 subgroups, and their functions were preliminarily analyzed. We found that some biological processes related to pregnancy, hormone secretion and immunity changed in the PE group. We also identified and analyzed the regulatory network of transcription factors (TFs) identified in the EVTs, among which 3 modules were decreased in the PE group. Then, through in vitro cell experiments, we found that in one of the modules, CEBPB and GTF2B may be involved in EVT dysfunction in PE. In conclusion, our study showed the different transcriptional profiles and regulatory modules in trophoblasts between placentas in the control and PE groups at the single-cell level; these changes may be involved in the pathological process of PE, providing a new molecular theoretical basis for preeclamptic trophoblast dysfunction.

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Partial least squares-based gene expression analysis in preeclampsia

Cited by 5 publications

References 25 publications

Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

Identification of key microRNAs and genes in preeclampsia by bioinformatics analysis

Trophoblast Cell Subtypes and Dysfunction in the Placenta of Individuals with Preeclampsia Revealed by Single-Cell RNA Sequencing

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