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  1. Article ; Online: The causal role of circulating immunity-inflammation in preeclampsia: A Mendelian randomization.

    Xue, Xiaolei / Guo, Chuanhui / Fan, Cuifang / Lei, Di

    Journal of clinical hypertension (Greenwich, Conn.)

    2024  

    Abstract: Patients with systemic autoimmune diseases, such as systemic lupus erythematosus, were at a higher risk for preeclampsia. The causal relationship between immunological inflammation and preeclampsia (PE) remains uncertain. We aimed to investigate the ... ...

    Abstract Patients with systemic autoimmune diseases, such as systemic lupus erythematosus, were at a higher risk for preeclampsia. The causal relationship between immunological inflammation and preeclampsia (PE) remains uncertain. We aimed to investigate the causal relationship between circulating immune inflammation and PE. Genetically predicted blood immune cells and circulating inflammatory proteins were identified using two genome-wide association studies (GWAS). We used a two-sample Mendelian randomization (MR) method to determine whether circulating immunological inflammation causes PE. Our findings indicated that ten immunophenotypes were identified to be significantly associated with PE risk: CD62L- Dendritic Cell Absolute Count, CD86+ myeloid Dendritic Cell %Dendritic Cell, CD62L- myeloid Dendritic Cell Absolute Count, CD86+ myeloid Dendritic Cell Absolute Count, CD62L- myeloid Dendritic Cell %Dendritic Cell, CD62L- CD86+ myeloid Dendritic Cell %Dendritic Cell, CD62L- CD86+ myeloid Dendritic Cell Absolute Count, CD16 on CD14+ CD16+ monocyte, HLA DR+ Natural Killer Absolute Count, and T cell Absolute Count. Ninety-one inflammation-related proteins had no statistically significant effect on PE following false discovery rate (FDR) correction. Certain proteins exhibited unadjusted low p-values that merited mention. These proteins include interleukin-10 (OR = 0.76, 95%CI = 0.63-0.93, p = .006), fibroblast growth factor 21 (OR = 1.23, 95%CI = 1.01-1.47, p = .035), and Caspase 8 (OR = 0.65, 95%CI = 0.50-0.85, p = .001). The ELISA analysis demonstrated elevated levels of FGF-21 and decreased levels of IL-10 and Caspase-8 in the plasma of patients with PE. These findings reveal that immunophenotypes and circulating inflammatory proteins may induce PE, confirming the importance of peripheral Immunity-Inflammation in PE. The discovery has the potential to lead to earlier detection and more effective treatment techniques.
    Language English
    Publishing date 2024-03-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2077222-1
    ISSN 1751-7176 ; 1524-6175
    ISSN (online) 1751-7176
    ISSN 1524-6175
    DOI 10.1111/jch.14775
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Single-Cell RNA Sequencing and Microarray Analysis Reveal the Role of Lipid-Metabolism-Related Genes and Cellular Immune Infiltration in Pre-Eclampsia and Identify Novel Biomarkers for Pre-Eclampsia.

    Liu, Yujie / Xu, Borui / Fan, Cuifang

    Biomedicines

    2023  Volume 11, Issue 8

    Abstract: Pre-eclampsia (PE) is a gestational hypertensive disorder that is characterized by hypertension and proteinuria, typically occurring after 20 weeks of gestation. Despite its global impact on pregnant women, the precise pathogenic mechanisms of PE remain ... ...

    Abstract Pre-eclampsia (PE) is a gestational hypertensive disorder that is characterized by hypertension and proteinuria, typically occurring after 20 weeks of gestation. Despite its global impact on pregnant women, the precise pathogenic mechanisms of PE remain unclear. Dysregulated lipid metabolism and immune cell infiltration contribute to PE development. Our study aimed to identify lipid-metabolism-related genes (LMRG-PEs) and investigate their association with immune infiltration. We utilized the "Seurat" R package for data quality control, cell clustering, and marker gene identification. The "SingleR" package enabled the matching of marker genes to specific cell types. Pseudotemporal ordering analysis was conducted using the "Monocle" package. Weighted correlation network analysis (WGCNA), gene set variation analysis (GSVA), and gene set enrichment analysis (GSEA) approaches were employed to explore lipid-metabolism-related genes, while potential targeted drugs were predicted using the drug-gene interaction database (DGIdb). Hub gene expression was validated through RT-qPCR. By analyzing single-cell RNA sequencing data, we identified and classified 20 cell clusters into 5 distinct types. Differential gene expression analysis revealed 186 DEGs. WGCNA identified 9 critical modules and 265 genes significantly associated with PE diagnosis, emphasizing the importance of the core genes
    Language English
    Publishing date 2023-08-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11082328
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Enzyme 15-Hydroxyprostaglandin Dehydrogenase Inhibits a Shift to the Mesenchymal Pattern of Trophoblasts and Decidual Stromal Cells Accompanied by Prostaglandin Transporter in Preeclampsia.

    Pang, Huiyuan / Lei, Di / Chen, Tingting / Liu, Yujie / Fan, Cuifang

    International journal of molecular sciences

    2023  Volume 24, Issue 6

    Abstract: Preeclampsia (PE) is a pregnancy complication beginning after 20 weeks of pregnancy that involves high blood pressure (systolic > 140 mmHg or diastolic > 90 mmHg), with or without proteinuria. Insufficient trophoblast invasion and abnormal ... ...

    Abstract Preeclampsia (PE) is a pregnancy complication beginning after 20 weeks of pregnancy that involves high blood pressure (systolic > 140 mmHg or diastolic > 90 mmHg), with or without proteinuria. Insufficient trophoblast invasion and abnormal decidualization are involved in PE development. However, whether unhealthy placenta and decidua have the same biological activities is unclear. The enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH; encoded by
    MeSH term(s) Pregnancy ; Humans ; Female ; Placenta/metabolism ; Trophoblasts/metabolism ; Pre-Eclampsia/metabolism ; Dinoprostone/metabolism ; Stromal Cells/metabolism ; Decidua/metabolism
    Chemical Substances 15-hydroxyprostaglandin dehydrogenase (EC 1.1.1.141) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2023-03-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24065111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The Enzyme 15-Hydroxyprostaglandin Dehydrogenase Inhibits a Shift to the Mesenchymal Pattern of Trophoblasts and Decidual Stromal Cells Accompanied by Prostaglandin Transporter in Preeclampsia

    Huiyuan Pang / Di Lei / Tingting Chen / Yujie Liu / Cuifang Fan

    International Journal of Molecular Sciences, Vol 24, Iss 5111, p

    2023  Volume 5111

    Abstract: Preeclampsia (PE) is a pregnancy complication beginning after 20 weeks of pregnancy that involves high blood pressure (systolic > 140 mmHg or diastolic > 90 mmHg), with or without proteinuria. Insufficient trophoblast invasion and abnormal ... ...

    Abstract Preeclampsia (PE) is a pregnancy complication beginning after 20 weeks of pregnancy that involves high blood pressure (systolic > 140 mmHg or diastolic > 90 mmHg), with or without proteinuria. Insufficient trophoblast invasion and abnormal decidualization are involved in PE development. However, whether unhealthy placenta and decidua have the same biological activities is unclear. The enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH; encoded by HPGD ) degrades prostaglandin, and prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, helps transport prostaglandin into cells. Whether 15-PGDH and PGT are involved in PE has not been researched. In this study, we investigated the shared pathogenesis of foetal placenta and maternal decidua from the perspective of epithelial–mesenchymal transition (EMT)/mesenchymal–epithelial transition (MET) and explored the combined effects of 15-PGDH and PGT on the EMT/MET of trophoblasts and decidual stromal cells (DSCs). Here, we demonstrated that placental development and decidualization both involved EMT/MET. In PE, both trophoblasts and DSCs show more epithelial patterns. Moreover, 15-PGDH expression was downregulated in the placentas but upregulated in the deciduas of PE patients. Inhibiting 15-PGDH promotes a shift to a mesenchymal pattern of trophoblasts and DSCs depending on the PGT-mediated transport of prostaglandin E2 (PGE2). In conclusion, our results showed that inhibiting 15-PGDH promotes a shift to the mesenchymal pattern of trophoblasts and DSCs and may provide a new and alternative therapy for the treatment of PE.
    Keywords preeclampsia ; placenta ; EMT ; decidua ; MET ; 15-PGDH ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Elevated PGT promotes proliferation and inhibits cell apoptosis in preeclampsia by Erk signaling pathway

    Huiyuan Pang / Di Lei / Jinfa Huang / Yuping Guo / Cuifang Fan

    Molecular and Cellular Probes, Vol 67, Iss , Pp 101896- (2023)

    2023  

    Abstract: Prostaglandins participate in maternal recognition of pregnancy, implantation and maintenance of gestation. Prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, might be involved in the pathogenesis of preeclampsia. In ... ...

    Abstract Prostaglandins participate in maternal recognition of pregnancy, implantation and maintenance of gestation. Prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, might be involved in the pathogenesis of preeclampsia. In preeclampsia (PE) patients’ placental tissue, we identified PGT by RNA sequencing, measured its expression pattern by quantitative real-time PCR and Western blot. PGT was found to be upregulated in preeclamptic placental tissue. The expression pattern of PGT in PE was double confirmed by eight Gene Expression Omnibus (GEO) databases. In abortion tissues at 6–8 weeks, we then observed the cellular location of PGT by Immunofluorescence technique (IF) and found PGT located in trophoblast cell of the placenta of early pregnancy. In vitro studies revealed that forced expression of PGT in HTR8/Sveno cell inhibited its apoptosis, but promoted its proliferation by activating Erk signaling. In vivo study, we used reduced uterine perfusion pressure (RUPP) rat model and L-NAME-induced preeclampsia-like rats to study the possible role of PGT in preeclampsia. And PGT was found to be upregulated in both preeclampsia rat models by Immunohistochemical (IHC) staining. Newly identified PGT plays an important role in trophoblast proliferation via Erk signaling, providing new insights for understanding the pathogenesis of PE.
    Keywords Preeclampsia ; PGT ; Proliferation ; Apoptosis ; Erk pathway ; Biology (General) ; QH301-705.5 ; Medicine ; R
    Language English
    Publishing date 2023-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Elevated PGT promotes proliferation and inhibits cell apoptosis in preeclampsia by Erk signaling pathway.

    Pang, Huiyuan / Lei, Di / Huang, Jinfa / Guo, Yuping / Fan, Cuifang

    Molecular and cellular probes

    2023  Volume 67, Page(s) 101896

    Abstract: Prostaglandins participate in maternal recognition of pregnancy, implantation and maintenance of gestation. Prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, might be involved in the pathogenesis of preeclampsia. In ... ...

    Abstract Prostaglandins participate in maternal recognition of pregnancy, implantation and maintenance of gestation. Prostaglandin transporter (PGT), as a candidate molecule of prostaglandin carriers, might be involved in the pathogenesis of preeclampsia. In preeclampsia (PE) patients' placental tissue, we identified PGT by RNA sequencing, measured its expression pattern by quantitative real-time PCR and Western blot. PGT was found to be upregulated in preeclamptic placental tissue. The expression pattern of PGT in PE was double confirmed by eight Gene Expression Omnibus (GEO) databases. In abortion tissues at 6-8 weeks, we then observed the cellular location of PGT by Immunofluorescence technique (IF) and found PGT located in trophoblast cell of the placenta of early pregnancy. In vitro studies revealed that forced expression of PGT in HTR8/Sveno cell inhibited its apoptosis, but promoted its proliferation by activating Erk signaling. In vivo study, we used reduced uterine perfusion pressure (RUPP) rat model and L-NAME-induced preeclampsia-like rats to study the possible role of PGT in preeclampsia. And PGT was found to be upregulated in both preeclampsia rat models by Immunohistochemical (IHC) staining. Newly identified PGT plays an important role in trophoblast proliferation via Erk signaling, providing new insights for understanding the pathogenesis of PE.
    MeSH term(s) Humans ; Pregnancy ; Female ; Rats ; Animals ; Placenta/metabolism ; Placenta/pathology ; Pre-Eclampsia/genetics ; Signal Transduction ; Cell Proliferation ; Apoptosis ; Prostaglandins/metabolism
    Chemical Substances Prostaglandins
    Language English
    Publishing date 2023-02-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 639082-1
    ISSN 1096-1194 ; 0890-8508
    ISSN (online) 1096-1194
    ISSN 0890-8508
    DOI 10.1016/j.mcp.2023.101896
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Retraction Note: Human Umbilical Cord Mesenchymal Stem Cells-Derived Exosomal MicroRNA-18b-3p Inhibits the Occurrence of Preeclampsia by Targeting LEP.

    Huang, Qin / Gong, Meng / Tan, Tuantuan / Lin, Yunong / Bao, Yan / Fan, Cuifang

    Nanoscale research letters

    2022  Volume 17, Issue 1, Page(s) 119

    Language English
    Publishing date 2022-12-09
    Publishing country United States
    Document type Retraction of Publication
    ZDB-ID 2253244-4
    ISSN 1556-276X ; 1931-7573
    ISSN (online) 1556-276X
    ISSN 1931-7573
    DOI 10.1186/s11671-022-03765-6
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  8. Article ; Online: Severe COVID-19 in a pregnant patient admitted to hospital in Wuhan.

    Yu, Ying / Fan, Cuifang / Bian, Junmei / YinShen

    International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics

    2020  Volume 150, Issue 2, Page(s) 262–263

    Keywords covid19
    Language English
    Publishing date 2020-07-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80149-5
    ISSN 1879-3479 ; 0020-7292
    ISSN (online) 1879-3479
    ISSN 0020-7292
    DOI 10.1002/ijgo.13232
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  9. Article ; Online: Role of CircCHD2 in the pathogenesis of gestational diabetes mellitus by regulating autophagy via miR-33b-3p/ULK1 axis.

    Bao, Yindi / Wu, Lianzhi / Liu, Yi / Fan, Cuifang / Zhang, Jun / Yang, Jing

    Placenta

    2023  Volume 145, Page(s) 27–37

    Abstract: Gestational diabetes mellitus (GDM) is a common pregnancy complication with a high incidence in women; however, its pathophysiology remains unknown. Our previous study suggested that the circCHD2/miR-33b-3p/ULK1 axis may be involved in GDM pathogenesis. ... ...

    Abstract Gestational diabetes mellitus (GDM) is a common pregnancy complication with a high incidence in women; however, its pathophysiology remains unknown. Our previous study suggested that the circCHD2/miR-33b-3p/ULK1 axis may be involved in GDM pathogenesis. However, the mechanism through which circCHD2 regulates GDM development requires further investigation. We found that high-glucose (HG, 25 mmol/L) significantly induced the expression of circCHD2, increased autophagy and apoptosis, and decreased cell viability in human placental trophoblast HTR-8/SVneo cells. In contrast, the downregulation of circCHD2 significantly attenuated the effects of HG on HTR-8/SVneo cells. MiR-33b-3p downregulated in the placenta of GDM patients was reduced by HG and detected as a target of circCHD2 using bioinformatics analysis, a dual-luciferase reporter assay, and qRT-PCR assay. Further studies showed that the inhibition of miR-33b-3p significantly blocked the effects of circCHD2 downregulation on cell viability, apoptosis, and autophagy in HG-treated HTR-8/SVneo cells. ULK1 is a target of miR-33b-3p, based on bioinformatics analysis, a dual-luciferase reporter assay, qRT-PCR assay, and Western blot analysis. Compared to miR-33b-3p, ULK1 is upregulated in the placenta of GDM patients. ULK1 overexpression notably blocked the effects of miR-33b-3p mimics on cell viability, apoptosis, and autophagy in HG-treated HTR-8/SVneo cells. These findings suggested that circCHD2 acts as an autophagy promoter via the miR-33b-3p/ULK1 axis to induce apoptosis in HTR-8/SVneo cells, suggesting that circCHD2 is a potential diagnostic and therapeutic target for GDM.
    MeSH term(s) Female ; Humans ; Pregnancy ; Autophagy/genetics ; Autophagy-Related Protein-1 Homolog/genetics ; Autophagy-Related Protein-1 Homolog/metabolism ; Cell Proliferation/physiology ; Diabetes, Gestational/genetics ; Diabetes, Gestational/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Luciferases/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Placenta/metabolism ; Trophoblasts/metabolism ; RNA, Circular/genetics ; RNA, Circular/metabolism
    Chemical Substances Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Intracellular Signaling Peptides and Proteins ; Luciferases (EC 1.13.12.-) ; MicroRNAs ; ULK1 protein, human (EC 2.7.11.1) ; MIRN33b microRNA, human ; RNA, Circular
    Language English
    Publishing date 2023-11-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 603951-0
    ISSN 1532-3102 ; 0143-4004
    ISSN (online) 1532-3102
    ISSN 0143-4004
    DOI 10.1016/j.placenta.2023.11.013
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