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Updated: Sep 21, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
RAR-Related Orphan Receptor: An Accelerated Preeclampsia Progression by Activating the JAK/STAT3 Pathway
1Department of Obstetrics, Zhangqiu District People's Hospital, Jinan, Shandong, China.
Purpose:
To investigate the effect and underlying mechanism of RAR related orphan receptor A (RORA) on preeclampsia (PE).
Materials And Methods:
Differentially expressed genes (DEGs) in four datasets were obtained by using the Venn diagram method. RORA mRNA and protein expressions were detected by qRT-PCR, western blot, and immunohistochemistry. HTR-8/SVneo cell viability, proliferation, invasion, migration, and angiogenesis were detected by CCK-8 assay, EdU assay, Transwell, wound healing assay, and tube formation assay, respectively. The concentration of Ang-1 in cells was assessed using available ELISA kit. Epithelial-mesenchymal transition, proliferation, and angiogenesis-related proteins were detected by western blot. GSEA analysis were performed for common DEGs, and the expression of enriched pathway-related proteins was also detected.
Results:
The expression of RORA was increased in PE tissue and HTR-8/SVneo cells. Silencing RORA could promote the migration, invasion, epithelial-mesenchymal transition, proliferation, and angiogenesis of hypoxia-treated HTR-8/SVneo cells. Mechanistically, RORA contributed to the deterioration of PE by activating the JAK2/STAT3 signaling pathway to promote cell proliferation, migration, invasion, and angiogenesis.
Conclusion:
RORA was up-regulated in PE and affected HTR-8/SVneo cell proliferation, invasion, migration, apoptosis, and angiogenesis via the JAK2/STAT3 signaling pathway. This provided a novel strategy for the prevention and treatment of PE.
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