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E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis
Xili Yang1, Xinyan Zhao1, Kaiwen Fu1
1Department of Anesthesiology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
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.
Insights
E2F2 exacerbates poststroke depression (PSD) by inhibiting hippocampal neurogenesis through the miR-1290/CBR1 pathway. Targeting this axis may offer new treatments for PSD.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Poststroke depression (PSD) involves depressive symptoms and cognitive decline.
- Hippocampal neurogenesis is crucial for cognitive function and is impaired in PSD.
Purpose of the Study:
- To investigate the regulatory role of E2F2 in hippocampal neurogenesis within a poststroke depression rat model.
- To elucidate the molecular mechanism involving E2F2, miR-1290, and CBR1 in PSD.
Main Methods:
- Established a rat model of PSD using middle cerebral artery occlusion (MCAO) and chronic unpredictable mild stress (CUMS).
- Assessed depressive behaviors and hippocampal neurogenesis markers (NeuN, BDNF).
- Quantified gene and protein expression (WB, RT-qPCR), performed chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays.
Main Results:
- PSD rats exhibited depressive behaviors and impaired hippocampal neurogenesis.
- E2F2 was upregulated in PSD rats; E2F2 knockdown improved depressive symptoms and neurogenesis.
- E2F2 promoted miR-1290 transcription, which in turn suppressed CBR1 expression.
- miR-1290 overexpression or CBR1 inhibition mimicked the neurogenesis-promoting effects of E2F2 knockdown.
Conclusions:
- E2F2 inhibits hippocampal neurogenesis in PSD via the miR-1290/CBR1 signaling axis.
- This pathway represents a potential therapeutic target for managing poststroke depression.
