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

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.