Hsp90aa1/JUN/Ccl2 regulatory axis mediates migration and differentiation of NSPCs, promoting the onset and progression of early post-ischemic stroke epilepsy.
Shuntong HuYongzhong TangXiaobo LiWenjun LiYini ZengMi JiangRu ChenPing ZhengLiang YangZhi SongDujie XieYiwei ChenYi YuanPublished in: Neurobiology of disease (2024)
Early-onset epilepsy following ischemic stroke is a severe neurological condition, the pathogenesis of which remains incompletely understood. Recent studies suggest that Neural stem/progenitor cells (NSPCs) play a crucial role in the disease process, yet the precise molecular mechanisms regulating NSPCs have not been thoroughly investigated. This study utilized single-cell transcriptome sequencing and bioinformatics analysis to identify disease-related genes, which were subsequently validated in both in vitro and in vivo experiments. The findings revealed that Hsp90aa1 (heat shock protein 90 kDa alpha, class A member 1), Jun proto-oncogene (JUN), and CC Motif Ligation 2 (Ccl2) constitute an important regulatory axis influencing the migration and differentiation of NSPCs, potentially impacting the onset and progression of early-onset epilepsy post-ischemic stroke. Additionally, the expression of Hsp90aa1 was found to influence the likelihood of seizure occurrence and the severity of brain ischemia.
Keyphrases
- heat shock protein
- early onset
- single cell
- late onset
- rna seq
- heat shock
- atrial fibrillation
- bioinformatics analysis
- temporal lobe epilepsy
- transcription factor
- high throughput
- poor prognosis
- risk assessment
- liver fibrosis
- gene expression
- liver injury
- cerebral ischemia
- multiple sclerosis
- resting state
- atomic force microscopy