Increased SUMO-1 expression in the unilateral rotenone-lesioned mouse model of Parkinson's disease

J. Weetman, M.B. Wong, S Sharry, A. Rcom-H'cheo-Gauthier, Weiping Gai, A Meedeniya, Dean Pountney

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    26 Citations (Scopus)


    Parkinson's disease (PD) is a neurodegenerative disease resulting from progressive loss of dopaminergic nigrostriatal neurons. α-Synuclein protein conformational changes, resulting in cytotoxic/aggregated proteins, have been linked to PD pathogenesis. We investigated a unilateral rotenone-lesioned mouse PD model. Unilateral lesion of the medial forebrain bundle for two groups of male C57 black mice (n= 5); adult (6-12 months) group and aged (1.75-2 years) group, was via stereotactic rotenone injection. After 2 weeks post-lesion, phenotypic Parkinsonian symptoms, resting tremor, postural instability, left-handed bias, ipsiversive rotation and bradykinesia were observed and were more severe in the aged group. We investigated protein expression profiles of the post-translational modifier, SUMO-1, and α-synuclein between the treated and control hemisphere, and between adult and aged groups. Western analysis of the brain homogenates indicated that there were statistically significant (p< 0.05) increases in several specific molecular weight species (ranging 12-190. kDa) of both SUMO-1 (0.75-4.3-fold increased) and α-synuclein (1.6-19-fold increase) in the lesioned compared to un-lesioned hemisphere, with the adult mice showing proportionately greater increases in SUMO-1 than the aged group.

    Original languageEnglish
    Pages (from-to)119-124
    Number of pages6
    JournalNeuroscience Letters
    Publication statusPublished - 7 Jun 2013


    • α-Synuclein
    • Parkinson's disease
    • Rotenone
    • SUMO


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