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<p>Poststroke depression (PSD) presents with persistent depressive symptoms and cognitive dysfunction. This study explored the regulatory mechanism of E2F2 in hippocampal neurogenesis in PSD. In a PSD rat model established by MCAO and CUMS, depressive behaviors (reduced sucrose preference, prolonged immobility time) and impaired hippocampal neurogenesis (decreased NeuN-positive cells and BDNF protein) were observed. BDNF, E2F2, CBR1, and miR-1290 were measured by WB and RT-qPCR. E2F2 enrichment on the miR-1290 promoter was assessed by Ch-IP assay. The bindings of E2F2 to the miR-1290 promoter and miR-1290 to the CBR1 3’-UTRwere validated using dual-luciferase reporter assays. Molecular analyses revealed that E2F2 was upregulated in PSD rats, and E2F2 knockdown alleviated depressive symptoms and neurogenesis deficits. Mechanistically, E2F2 bound to the miR-1290 promoter and enhance miR-1290 transcription, while miR-1290 targeted the 3’-UTR of CBR1 and suppress its expression. Rescue experiments confirmed that miR-1290 overexpression or CBR1 inhibition counteracted the neurogenesis-promoting effects of E2F2 knockdown. In conclusion, E2F2 inhibits hippocampal neurogenesis in PSD via the miR-1290/CBR1 axis, providing a potential therapeutic target for treating PSD.</p>

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E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis

  • 期刊论文

  • 发表日期：

    2025年11月27日

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  • Xili Yang,
  • Xinyan Zhao,
  • Kaiwen Fu,
  • Binquan Tang,
  • Xiaohong Du,
  • Huiying Liu,
  • Shuchun Yu,
  • Fan Xiao

摘要

Poststroke depression (PSD) presents with persistent depressive symptoms and cognitive dysfunction. This study explored the regulatory mechanism of E2F2 in hippocampal neurogenesis in PSD. In a PSD rat model established by MCAO and CUMS, depressive behaviors (reduced sucrose preference, prolonged immobility time) and impaired hippocampal neurogenesis (decreased NeuN-positive cells and BDNF protein) were observed. BDNF, E2F2, CBR1, and miR-1290 were measured by WB and RT-qPCR. E2F2 enrichment on the miR-1290 promoter was assessed by Ch-IP assay. The bindings of E2F2 to the miR-1290 promoter and miR-1290 to the CBR1 3’-UTRwere validated using dual-luciferase reporter assays. Molecular analyses revealed that E2F2 was upregulated in PSD rats, and E2F2 knockdown alleviated depressive symptoms and neurogenesis deficits. Mechanistically, E2F2 bound to the miR-1290 promoter and enhance miR-1290 transcription, while miR-1290 targeted the 3’-UTR of CBR1 and suppress its expression. Rescue experiments confirmed that miR-1290 overexpression or CBR1 inhibition counteracted the neurogenesis-promoting effects of E2F2 knockdown. In conclusion, E2F2 inhibits hippocampal neurogenesis in PSD via the miR-1290/CBR1 axis, providing a potential therapeutic target for treating PSD.