Abnormal changes in voltage-gated sodium channels subtypes Na_V1.1, Na_V1.2, Na_V1.3, Na_V1.6 and CaM/CaMKII pathway in low-grade astrocytoma.

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_V1.3, Na_V1.6 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 and immunohistochemistry. Furthermore, double-labeling immunofluorescence results showed that Na_V1.3/Na_V1.6 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.

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