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.
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.
Purpose
To investigate the effect and underlying mechanism of RAR related orphan receptor A (RORA) on preeclampsia (PE). Materials and
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.