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Background <p>N6-methyladenosine (m6A) methylation modification plays an essential role in the molecular pathogenesis of preeclampsia (PE). This study aimed to explore m6A modification in in vitro PE model, involving RNA binding motif protein 15 (RBM15) and FBJ murine osteosarcoma viral oncogene homolog B (FOSB).</p> Methods <p>PE was induced by lipopolysaccharide (LPS) in HTR8/SVneo cells. Real-time quantification PCR was used for mRNA detection and Western blotting was used for protein detection. Cell cytokines were examined using enzyme-linked immunosorbent assay. Cell functions were evaluated using EdU assay, flow cytometry, and transwell assay. RNA immunoprecipitation assay and dual-luciferase reporter assay were utilized for validating molecular interaction.</p> Results <p>FOSB was highly expressed in placenta tissues from PE patients. Functionally, LPS-induced inflammation, proliferation inhibition, cell apoptosis and migration suppression were significantly abolished following FOSB knockdown. RBM15 upregulated FOSB expression via inducing m6A modification of FOSB mRNA. YTH N6-methyladenosine RNA-binding protein 1 (YTHDF1) acted as an m6A reader protein, and RBM15 enhanced the binding between YTHDF1 and FOSB. RBM15 knockdown relieved LPS-caused trophoblast cell injury by inhibiting FOSB.</p> Conclusion <p>These results collectively suggested that RBM15 accelerated trophoblast cell dysfunction via mediating m6A modification of FOSB mRNA through the identification by YTHDF1.</p>

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RBM15 mediates m6A methylation modification of FOSB mRNA to promote dysfunction of trophoblast cells-a potential link to preeclampsia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月21日

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  • Yan Li,
  • Fei Li,
  • Qian Gao

摘要

Background

N6-methyladenosine (m6A) methylation modification plays an essential role in the molecular pathogenesis of preeclampsia (PE). This study aimed to explore m6A modification in in vitro PE model, involving RNA binding motif protein 15 (RBM15) and FBJ murine osteosarcoma viral oncogene homolog B (FOSB).

Methods

PE was induced by lipopolysaccharide (LPS) in HTR8/SVneo cells. Real-time quantification PCR was used for mRNA detection and Western blotting was used for protein detection. Cell cytokines were examined using enzyme-linked immunosorbent assay. Cell functions were evaluated using EdU assay, flow cytometry, and transwell assay. RNA immunoprecipitation assay and dual-luciferase reporter assay were utilized for validating molecular interaction.

Results

FOSB was highly expressed in placenta tissues from PE patients. Functionally, LPS-induced inflammation, proliferation inhibition, cell apoptosis and migration suppression were significantly abolished following FOSB knockdown. RBM15 upregulated FOSB expression via inducing m6A modification of FOSB mRNA. YTH N6-methyladenosine RNA-binding protein 1 (YTHDF1) acted as an m6A reader protein, and RBM15 enhanced the binding between YTHDF1 and FOSB. RBM15 knockdown relieved LPS-caused trophoblast cell injury by inhibiting FOSB.

Conclusion

These results collectively suggested that RBM15 accelerated trophoblast cell dysfunction via mediating m6A modification of FOSB mRNA through the identification by YTHDF1.