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The role of glycogen synthase kinase-3beta in alpha-synuclein-evoked tau phosphorylation

100%

Gassowska M. , Czapski G. A. , Adamczyk A.

nr Suppl.1

Hyperphosphorylation of tau is involved in the pathomechanism of neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. Recent studies suggested the significance of alpha-synuclein (ASN) in tau phosphorylation, however, the molecular mechanism responsible for ASN-mediated tau modification remains to be elucidated. In this study, we investigated the role of extracellular ASN in tau phosphorylation in PC12 dopaminergic cells and the involvement of glycogen synthase kinase-3 beta (GSK-3β) and cyclin-dependent kinase 5 (CDK5) in ASN-induced tau modification and cell death. We found that exogenously added ASN (10 µM) stimulates the phosphorylation of tau at Ser396 in PC12 cells. A specific GSK-3β inhibitor (SB-216763) prevented ASN-evoked tau hyperphosphorylation without effect of CDK5 inhibitors. Furthermore, we found that ASN enhanced of GSK-3β protein level and activity. Cell viability determined by MTT assay and Hoechst 33258 staining showed that ASN induced PC12 cell death that presented typical apoptotic morphology. SB-216763 prevented apoptotic cell death evoked by ASN. Concluding, extracellular ASN is involved in GSK-3β-dependent tau modulation and its proapoptotic effect might be mediated at least in part by GSK-3β-catalysed tau phosphorylation and cytoskeleton destabilisation. Supported by a grant from The National Science Centre 2012/05/B/NZ3/02047.

Ceramide/sphingosine-1-phosphate in cellls survival and death: implication in Alzheimer’s disease

100%

Strosznajder R. P. , Czubowicz K. , Gassowska M. , Cieslik M.

nr Suppl.1

Ceramide and sphingosine-1-phosphate (S1P) are very active sphingolipid messengers which play a crucial role in regulation of neuronal cells survival and death. Alternation of ceramide/S1P rheostat is related to several pathological disorders including Alzheimer’s disease. Ceramides are involved in cells proliferation, differentiation and apoptotic death, while S1P enhances cell proliferation and antagonizes apoptosis. S1P regulates cellular processes by binding to five specific G protein coupled-receptors (S1PR1-5). The aim of the study was to investigate the molecular processes of neuronal death evoked by ceramide and the role of S1P in neuroprotection. Our study indicated that ceramide enhanced significantly the level of free radicals and decreased neuronal cells (SHSY5Y) viability through inhibition of PI3-K/Akt pathway. Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) gene expression. Exogenously added S1P increased the viability of cells through S1PR (1-3) receptors-dependent mechanism. S1P also increased Bcl-2 gene expression and decreased the gene expression of Hrk protein. Summarizing, our study indicated that the action of ceramide and S1P on mitochondria may control neuronal fate and may play a crucial role in neurodegeneration and neuroprotection.

The effect of NaF on the Na+/H+ exchanger in unstimulated human platelets

100%

Gassowska M. , Dolegowska B. , Chlubek D.

tom 53

nr Supplement 1

Extracellular alpha-synuclein induces calpain-dependent overactivation of cyclin-dependent kinase 5 in PC12 cells

88%

Adamczyk A. , Gassowska M. , Wilkaniec A. , Cieslik M. , Czapski G. A.

nr Suppl.1