Session Information
Date: Monday, October 8, 2018
Session Title: Parkinson's Disease: Pathophysiology
Session Time: 1:15pm-2:45pm
Location: Hall 3FG
Objective: To investigate the expression of Semaphorin6D (SEMA6D) and its interaction with Plexin-A1 in cellular Parkinson’s disease(PD) models induced by α-synuclein and rotenone.
Background: In order to uncover the molecular pathological process in Parkinson’s disease (PD) ,we employed a microarray analysis upon the alpha-synuclein oligomer induced cellular PD model and investigate the significant differentially expressed genes(DEGs) screened from the microarray analysis.
Methods: SY-SH5Y cells cultured in vitro were divided into three groups:normal control group, α-synuclein oligomer-induced group, rotenone-induced group.The last two groups were treated with α-synuclein oligomer and rotenone respectively to establish the cellular PD models. The mRNA levels of SEMA6D and plexin-A1 were evaluated using real-time polymerase chain reaction analysis(rt-PCR), and the determinations had also been made on related proteins by Western blot analysis. The interaction between SEMA6D and Plexin-A1 was validated by co-immunoprecipitation. Immunofluorescence and co-focusing experiment were used to investigate the co-location of SEMA6D and PlexinA1 inside the cell.
Results: As the result showed, the expression of SEMA6D was significantly decreased in cellular PD model. KEGG Pathway analysis showed that SEMA6D was closely related to the network of MARK pathway. Comparing with the normal control group, the expressions of SEMA6D in cellular PD model groups were down-regulated obviously. Immunoprecipitation analysis and Immunofluorescence co-localization analysis comfirmed that the association of SEMA6D with Plexin-A1 was reversed in PD models.
Conclusions: α-synuclein and rotenone treatments inhibit expression of SEMA6D and its interaction with Plexin-A1. The decline of their interaction could trigger the MAPK signaling pathway, which is associated with the progress of PD.Our results suggest that SEMA6D is a critical factor in the pathogenesis of PD, and therefore could be an important drug target for novel treatments towards PD.
To cite this abstract in AMA style:
X. Yingyu. Alpha-synuclein oligomer and rotenone treatments injury the dopaminergic neuron via inhibiting the expression of gene SEMA6D [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/alpha-synuclein-oligomer-and-rotenone-treatments-injury-the-dopaminergic-neuron-via-inhibiting-the-expression-of-gene-sema6d/. Accessed June 14, 2025.« Back to 2018 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/alpha-synuclein-oligomer-and-rotenone-treatments-injury-the-dopaminergic-neuron-via-inhibiting-the-expression-of-gene-sema6d/