Abstract
Long non‐coding RNAs (lncRNAs) have been implicated in the regulation of gene expression at various levels. However, to date, the expression profile of lncRNAs in status epilepticus (SE) was unclear. In our study, the expression profile of lncRNAs was investigated by high‐throughput sequencing based on a lithium/pilocarpine‐induced SE model in immature rats. Furthermore, weighted correlation network analysis (WGCNA), gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to construct co‐expression networks and establish functions of the identified hub lncRNAs in SE. The functional role of a hub lncRNA (NONRATT010788.2) in SE was investigated in an in vitro model. Our results indicated that 7082 lncRNAs (3522 up‐regulated and 3560 down‐regulated), which are involved in cell proliferation, inflammatory responses, angiogenesis and autophagy, were dysregulated in the hippocampus of immature rats with SE. Additionally, WGCNA identified 667 up‐regulated hub lncRNAs in turquoise module that were involved in apoptosis, inflammatory responses and angiogenesis via regulation of HIF‐1, p53 and chemokine signalling pathways and via inflammatory mediator regulation of TRP channels. Knockdown of an identified hub lncRNA (NONRATT010788.2) inhibited neuronal apoptosis in vitro. Taken together, our study is the first to demonstrate the expression profile and potential function of lncRNAs in the hippocampus of immature rats with SE. The defined hub lncRNAs may participate in the pathogenesis of SE via lncRNA‐miRNA‐mRNA network.
Highlights
Status epilepticus (SE) is the second‐ most common neurological disorder, with an annual incidence of 10‐41 cases in a population of 100 000.1,2 As irreversible cerebral damage occurs, it is necessary to promptly stop convulsions of SE and prevent their recurrence.[3]
LncRNAs may play a crucial role in SE as they are involved in regu‐ lation of gene expression at the epigenetic, transcriptional or post‐ transcriptional level.[7,8]
Functional prediction indicated that the dysregulated Long non‐coding RNAs (lncRNAs) were involved in cell proliferation, inflammatory responses, angiogenesis and au‐ tophagy through regulation of cGMP, MAPK and Rap[1] signalling pathways
Summary
Status epilepticus (SE) is the second‐ most common neurological disorder, with an annual incidence of 10‐41 cases in a population of 100 000.1,2 As irreversible cerebral damage occurs, it is necessary to promptly stop convulsions of SE and prevent their recurrence.[3] The morbidity and mortality of SE are determined by the duration of ep‐ ileptic activity, rapid identification of the cause of SE, and age and comorbidity of the patients.[4] During SE development, hypoxic stress and inflammatory stress are initiated together with microglia and mac‐ rophage activation, which induce several cerebral processes resulting in neuron cell apoptosis, and further severe neuronal damage.[5,6]. The functional role of a hub lncRNA (NONRATT010788.2) in SE was investigated in an in vitro model
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