ArticleNeural regeneration research2014
Increased expression of Notch1 in temporal lobe epilepsy: animal models and clinical evidence.
Article in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Cross-species transcriptomic analysis of rodent model fidelity to human mesial temporal lobe epilepsy.Nature communications · 2026Article
- Notch signaling inhibition attenuates epileptogenesis and hippocampal damage without altering mossy fiber sprouting in adolescent rats post-status epilepticus.Frontiers in molecular neuroscience · 2026Article
- Transcriptome analysis in an AEG‑1‑deficient neuronal HT22 cell line.Experimental and therapeutic medicine · 2022Article
- The role of peptidyl-prolyl isomerase Pin1 in neuronal signaling in epilepsy.Frontiers in molecular neuroscience · 2022Review
- Silencing of microRNA-146a alleviates the neural damage in temporal lobe epilepsy by down-regulating Notch-1.Molecular brain · 2019Article
- Discrepancies of Notch 1 receptor during development of chronic seizures.Journal of cellular physiology · 2019Article
- Chronically dysregulated NOTCH1 interactome in the dentate gyrus after traumatic brain injury.PloS one · 2017Article
- Cysteinyl Leukotrienes as Potential Pharmacological Targets for Cerebral Diseases.Mediators of inflammation · 2017Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temporal lobe epilepsy is associated with astrogliosis. Notch1 signaling can induce astrogliosis in glioma. However, it remains unknown whether Notch1 signaling is involved in the pathogenesis of epilepsy. This study investigated the presence of Notch1, hairy and enhancer of split-1, and glial fibrillary acidic protein in the temporal neocortex and hippocampus of lithium-pilocarpine-treated rats. The presence of Notch1 and hairy and enhancer of split-1 was also explored in brain tissues of patients with intractable temporal lobe epilepsy. Quantitative electroencephalogram analysis and behavioral observations were used as auxiliary measures. Results revealed that the presence of Notch1, hairy and enhancer of split-1, and glial fibrillary acidic protein were enhanced in status epilepticus and vehicle-treated spontaneous recurrent seizures rats, but remain unchanged in the following groups: control, absence of either status epilepticus or spontaneous recurrent seizures, and zileuton-treated spontaneous recurrent seizures. Compared with patient control cases, the presences of Notch1 and hairy and enhancer of split-1 were upregulated in the temporal neocortex of patients with intractable temporal lobe epilepsy. Therefore, these results suggest that Notch1 signaling may play an important role in the onset of temporal lobe epilepsy via astrogliosis. Furthermore, zileuton may be a potential therapeutic strategy for temporal lobe epilepsy by blocking Notch1 signaling.
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