Signature of Aberrantly Expressed microRNAs in the Striatum of Rotenone-Induced Parkinsonian Rats.

摘要: Parkinson’s disease (PD) is a highly complex brain disorder regarding clinical presentation, pathogenesis, and therapeutics. The cardinal motor signs, i.e., rigidity, bradykinesia, unilateral tremors, arise in consequence of progressive neuron death during the prodromal phase. Although multiple transmission systems are involved neurobiology, patients will cross line between early stage diagnosed PD when they had lost half dopaminergic nigrostriatal cells. As neurons continue to die ascending neuroaxis, face more disabling with nonmotor signs. Shedding light on molecular mechanisms an urgent need for understanding pathogenesis projecting This work examined expression microRNAs striatum parkinsonian rats chronically exposed rotenone (2.5 mg/Kg, i.p., daily 10 days). Rotenone caused deficits, loss TH(+) cells pathway, marked microgliosis. rat was at 26 days after last injection, quantification microRNAs, miR-7, miR-34a, miR-26a, miR-132, miR-382, Let7a, by qPCR. Parkinsonian presented significant increase miR-26a miR-34a (1.5 2.2 fold, respectively, P < 0.05), while miR-7 (0.5 P < 0.05) Let7a were downregulated. reports first time aberrantly expressed rotenone-induced rats, suggesting that this dysregulation may contribute pathogenesis. Beyond revealing new clues neurodegeneration, our findings might prime further studies targeting miRNAs neuroprotection or even diagnosis proposal.