Reduce heat shock proteins 70 cell model of Parkinsons disease -synuclein in the toxicity.doc

 PAGE \* MERGEFORMAT 13 Reduce heat shock proteins 70 cell model of Parkinson’s disease -synuclein in the toxicity [Abstract] Objective To evaluate the result of HSP70 @ - synuclein overexpression or mutation of Parkinson’s disease (PD) cell model and its mechanism. Overexpression was constructed wild type and PD-related mutant (A53T) @ - synuclein plasmid was transfected into human neuroblastoma cells (SH-SY5Y) cells have PD cell model; and expression in transfected cell models, HSP70 plasmid. transfection was detected by Western blot of HSP70 cell model @ - synuclein expression changes; by MTT assay after transfection cell model of HSP70 activity. Results HSP70 after transfection, cell model @ - synuclein expression decreased cell activity increased. Conclusion HSP70 by lowering @ - synuclein expression cell model of PD to play a protective role. [Keywords:] @ - synuclein; Heat Shock Protein 70; over-expression @ - Synuclein is a presynaptic expression in the central nervous system, soluble protein, can regulate membrane stability and neuronal plasticity and other physiological functions. Evidence suggests that @ - synuclein gene over-expression or mutation can cause @ - synuclein misfolded, toxic protein oligomers and the formation of polymer, its structure and dysfunction, which initiates a cascade of damage caused by dopaminergic system, leading to Parkinson’s disease (PD) . studies suggest that neuroprotective agents may be the treatment of PD, a new way, and heat shock protein 70 (HSP70) is one of them. HSP70 is a molecular chaperone family member, as an important stress protein, can interactions with misfolded proteins, preventing the formation of aggregates; In addition, HSP70 also helps misfolded protein degradation (1,2). in Drosophila and yeast PD model, we found, HSP70 can reduce @ - synuclein induced toxicity and neuronal apoptosis (3,4), and HSP70 inhibit the @ - synuclein may be related to toxicity and @ - synuclein interaction, stop @