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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Mitochondrial genetic landscape and its correlation with immune cell infiltration in preeclampsia: Insights from
Xunjia Ye1, Jieying Yu2, Youyuan Zhuo2
1Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Guangdong Second Provincial General Hospital, School of Medicine, Jinan University, Guangzhou 510317, China; International Joint Laboratory for Embryonic Development & Prenatal Medicine, Division of Histology and Embryology, School of Medicine, Jinan University, Guangzhou 510632, China.
Insights
This study identifies key mitochondria-related genes (MRGs) involved in preeclampsia (PE) and their link to the immune microenvironment. One gene, CYP11A1, shows potential as a biomarker for HELLP syndrome in PE patients.
Area of Science:
- Reproductive biology and genetics
- Maternal-fetal medicine
- Mitochondrial biology
Background:
- Preeclampsia (PE) is a major cause of maternal and perinatal complications.
- Mitochondrial dysfunction in the placenta is implicated in PE pathogenesis.
- The precise role of mitochondria-related genes (MRGs) in PE requires further elucidation.
Purpose of the Study:
- To identify and characterize MRGs associated with preeclampsia.
- To explore the regulatory mechanisms and biological pathways involved in PE.
- To investigate the potential of MRGs as diagnostic or prognostic biomarkers.
Main Methods:
- Differential gene expression analysis of MRGs using GEO datasets (GSE114691, GSE190971).
- LASSO regression for MRG selection and ROC curve analysis for model validation (GSE75010, GSE25906).
- GSEA, correlation analysis with immune cell infiltration, and single-cell sequencing were employed.
Main Results:
- Five hub MRGs (MOCS1, CYP11A1, GATM, SFXN3, BCL2L11) demonstrated high diagnostic accuracy for PE and correlated with immune cell infiltration.
- CYP11A1 expression was upregulated in PE placentas, particularly in extravillous trophoblasts.
- CYP11A1 showed an association with Hemolysis, Elevated Liver enzymes, and Low platelets (HELLP) syndrome.
Conclusions:
- Mitochondria-related genes and their interaction with the placental immune microenvironment are crucial in PE development.
- CYP11A1 emerges as a potential biomarker for HELLP syndrome.
- These findings offer new insights into PE pathophysiology and potential therapeutic targets.
Background:
Preeclampsia (PE), a hypertensive pregnancy disorder, remains a leading cause of maternal and perinatal morbidity and mortality. Mitochondria-related placental metabolic dysfunction is implicated in PE, but its mechanistic role is unclear. This study aimed to identify mitochondria-related genes (MRGs) and their possible regulatory mechanisms in PE.
Methods:
Differentially expressed mitochondria-related genes (MRGs) of PE were identified from Gene Expression Omnibus (GEO) dataset GSE114691 and GSE190971. LASSO regression analysis was used to screen key MRGs. Datasets GSE75010 and GSE25906 were used to validate the efficiency of the MRGs predictive model via receiver operating characteristic (ROC) curve analysis. Gene set enrichment analysis (GSEA) was conducted to verify underlying biological pathways in PE. Furthermore, we investigated the correlation analysis of MRGs and immune cell infiltration, as well as the association between the MRGs and clinical features. Single-cell sequencing analysis and immunofluorescence staining were used to verify the expression of critical gene in the placenta.
Results:
Five hub MRGs (MOCS1, CYP11A1, GATM, SFXN3, and BCL2L11) showed high diagnostic accuracy for PE and correlated with immune cell infiltration. CYP11A1 was further associated with Hemolysis, Elevated Liver enzymes, Low platelets (HELLP) syndrome and predominantly expressed in extravillous trophoblasts, with upregulated expression in PE placenta.
Conclusion:
The interaction between MRGs with the immune microenvironment might be vital in the development of PE. Among 5 hub MRGs, CYP11A1 might be a potential biomarker of HELLP syndrome. These findings provide novel insights into the underlying pathophysiology of PE and the discovery of new therapeutic targets.
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