Jing Guo1, Heng Wang1, Qian Wang1, Yangmei Chen1, Shengli Chen2. 1. Department of Neurology, The Affiliated Second Hospital of Chongqing Medical University 76 Linjiang Road, Chongqing, 400010, China. 2. Chongqing Three Gorges Central Hospital Chongqing, China.
Abstract
OBJECTIVE: The mechanisms underlying the pathogenesis of intractable epilepsy (IE) are still unclear. This study aimed to investigate the role of phosphorylation of Cyclase Response Element Binding Protein (p-CREB)/microRNA-132 (miR-132) signal pathway in the epileptogenesis. METHODS: Temporal lobe epilepsy (TLE) was induced in rodents, and the brain tissues were collected. P-CREB expression was detected by Western blot assay and immunochemistry at 6 h, 24 h, 3 d, 7 d, 14 d, 30 d and 60 d after induced status epilepsy (SE), respectively, and in patients with TLE. The expression of miR-132 was detected by RT-PCR. RESULTS: The p-CREB and miR-132 were highly expressed in both rats and patients with TLE as compared to controls. CONCLUSIONS: The expression of p-CREB and miR-132 increases in epilepsy rats and patients, suggesting a possible pathogenetic role of p-CREB and miR-132 in TLE via modulating the dendritic plasticity.
OBJECTIVE: The mechanisms underlying the pathogenesis of intractable epilepsy (IE) are still unclear. This study aimed to investigate the role of phosphorylation of Cyclase Response Element Binding Protein (p-CREB)/microRNA-132 (miR-132) signal pathway in the epileptogenesis. METHODS:Temporal lobe epilepsy (TLE) was induced in rodents, and the brain tissues were collected. P-CREB expression was detected by Western blot assay and immunochemistry at 6 h, 24 h, 3 d, 7 d, 14 d, 30 d and 60 d after induced status epilepsy (SE), respectively, and in patients with TLE. The expression of miR-132 was detected by RT-PCR. RESULTS: The p-CREB and miR-132 were highly expressed in both rats and patients with TLE as compared to controls. CONCLUSIONS: The expression of p-CREB and miR-132 increases in epilepsyrats and patients, suggesting a possible pathogenetic role of p-CREB and miR-132 in TLE via modulating the dendritic plasticity.
Entities:
Keywords:
Temporal lobe epilepsy; microRNA-132; mossy fiber sprouting; phosphorylation of cyclase response element binding protein
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