N. Mamulashvili 1, M. Chikviladze 1, L. Shanshiashvili 1,2, D. Mikeladze 1, 2
1 Institute of Chemical Biology, Ilia State University, Tbilisi, Georgia;
2 Department of Biochemistry, I.Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia;
Abstract: Previous studies showed that neuropathological conditions in the CNS, such as brain trauma, infection by human immunodeficiency virus (HIV), multiples sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD) are associated with accumulation of glutamate in the extracellular space, caused by reduced glutamate uptake and/or increased glutamate release by astrocytes. Much evidence suggests that MBP(Myelin Basic Protein) may be an autoantigen candidate in MS. MBP exhibits charge microheterogeneity as a result of post-translational modifications such as phosphorylation, deamidation, deimination, arginine methylation, and N-terminal acylation. It was hypothesized that MBP could change the inflammatory response in astrocytes. The aim of our work was to investigate the effects of MBP charge isomers on glutamate uptake and release by astrocytes.
The study found that C8 and C1 MBP differently act on the uptake and release of glutamate in astrocytes: nonmodified C1 MBP increases the uptake of glutamate and does not change the release, whereas C8 decreases the release of glutamate, but does not alter the uptake.