Abnormal changes in voltage-gated sodium channels subtypes NaV1.1, NaV1.2, NaV1.3, NaV1.6 and CaM/CaMKII pathway in low-grade astrocytoma

作者：Guan, Gefei; Zhao, Mingyi; Xu, Xiaoxue; Boczek, Tomasz; Mao, Xiaoyuan; Li, Zhi; Gao, Qinghua; Li, Jianing; Zhao, Dongyi; Niu, Wanting; Lei, Liming^*; Guo, Feng^*

来源：Neuroscience Letters, 2018, 674: 148-155.

DOI：10.1016/j.neulet.2018.03.047

• Seizure
• Low-grade astrocytoma
• VGSCs
• CaM
• CaMKII

Epileptic seizures are the main clinical manifestation of low-grade astrocytoma. Voltage-gated sodium channels (VGSCs) play a crucial role in epilepsy. Until now, the role of VGSCs and the relationships between calmodulin (CaM)/CaM-dependent protein kinase II (CaMKII) and VGSCs in low-grade astrocytoma have not been demonstrated. In our study, the protein expression of Na(V)1.3, Na(V)1.6 and CaM was significantly increased in the tumor compared to control tissue, while the level of p-CaMKII/CaMKII was significantly decreased in the tumor group as determined by Western Blotting and immunohistochemistry. Furthermore, double-labeling immuno-fluorescence results showed that Na(V)1.3/Na(V)1.6 and CaM co-localization was significantly increased in the tumor group compared to control tissue. This study represents the first evidence of the abnormal changes in VGSCs subtypes and CaM/CaMKII pathway in human brain low-grade astrocytoma, providing new potential targets for molecular therapies of this disease.

• 出版日期2018-5-1
• 单位中南大学; 广东省人民医院; 中国医科大学; 广东省心血管病研究所