ArticleMammalian genome : official journal of the International Mammalian Genome Society2025
E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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