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LncRNA Mir155hg contributes to hippocampal injury in status epilepticus rats through miR-155/Socs1/NF-κΒ signaling
Yangmei Xie1, Ming Wang2, Binyuan Xu3
1Department of Neurology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Background:
Neuroinflammation contributes to cognitive deficits in status epilepticus (SE). The lncRNA Mir155hg has been identified as a key regulator of inflammation, but its role in SE remains unclear.
Methods:
Mir155hg was knocked down using the adeno-associated virus (AAV) in the rat models of SE. Cognitive function and neuronal damage were assessed using Morris Water Maze and Nissl staining. Inflammatory cytokines (TNF-α, IL-1β) and NF-κB pathway activity were measured by Western blot. Mechanistic insights into Mir155hg-mediated NF-κB regulation were investigated via dual-luciferase assays and co-immunoprecipitation analysis.
Results:
Our findings demonstrated that elevated level of Mir155hg was positively correlated with upregulation of TNF-α and IL-1β both in vivo and in vitro. Knockdown of Mir155hg reduced hippocampal inflammation and NF-κB activation. Mechanistically, Mir155hg acted as a competing endogenous RNA to sequester miR-155, thereby suppressing the expression of Socs1, an E3 ligase targeting NF-κB p65 for degradation. Co-immunoprecipitation analysis confirmed the interaction between NF-κB p65 and Socs1.
Conclusions:
Mir155hg exacerbates SE-related neuroinflammation via the miR-155/Socs1/NF-κB axis. Targeting this pathway may mitigate SE-induced neuronal injury and cognitive deficits.
Insights
The long non-coding RNA Mir155hg worsens neuroinflammation in status epilepticus (SE) by inhibiting the miR-155/Socs1 pathway, leading to cognitive deficits. Targeting this axis may reduce SE-induced brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Neuroinflammation is a key factor in cognitive impairment following status epilepticus (SE).
- The long non-coding RNA (lncRNA) Mir155hg is implicated in inflammatory processes, but its specific role in SE pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of lncRNA Mir155hg in SE-induced neuroinflammation and cognitive deficits.
- To elucidate the molecular mechanisms by which Mir155hg influences inflammatory pathways in the context of SE.
Main Methods:
- Utilized adeno-associated virus (AAV) mediated knockdown of Mir155hg in rat models of SE.
- Assessed cognitive function and neuronal damage using the Morris Water Maze and Nissl staining.
- Quantified inflammatory cytokines (TNF-α, IL-1β) and NF-κB pathway activation via Western blot; explored molecular interactions using dual-luciferase assays and co-immunoprecipitation.
Main Results:
- Elevated Mir155hg levels correlated positively with increased TNF-α and IL-1β expression in SE models.
- Knockdown of Mir155hg significantly reduced hippocampal inflammation and NF-κB pathway activation.
- Mir155hg functions as a competing endogenous RNA (ceRNA), sequestering miR-155 and thereby decreasing Socs1 expression, which normally targets NF-κB p65 for degradation.
Conclusions:
- Mir155hg exacerbates SE-related neuroinflammation and cognitive deficits through the miR-155/Socs1/NF-κB signaling axis.
- Inhibition of the Mir155hg pathway presents a potential therapeutic strategy to mitigate SE-induced neuronal injury and cognitive impairments.
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