[No authors listed]
The present study aimed to investigate the effect of microRNAâ183 (miRâ183) on substantia nigra neurons by targeting oncostatin M receptor (OSMR) in a mouse model of Parkinson's disease (PD). The positive expression rates of OSMR and the apoptosis of substantia nigra neurons were detected by immunohistochemistry and terminal deoxynucleotidyl transferaseâmediated dUTPâbiotin nick endâlabeling, respectively. Substantia nigra neurons in normal and PD mice were cultured in vitro. The association between miRâ183 and OSMR was verified using a dual luciferase reporter gene assay. The expression of miRâ183 and the phosphoinositide 3âkinaseâAkt signaling pathwayâassociated genes were detected by reverse transcriptionâquantitative polymerase chain reaction and western blot analysis, respectively. Cell apoptosis was detected by flow cytometry. OSMR is the target gene of miRâ183. The number of OSMRâpositive cells and the apoptotic rate of substantia nigra neurons were increased in the PD group. Neurons transfected with miRâ183 mimic exhibited elevated expression levels of miRâ183, Bâcell lymphoma 2 (Bclâ2)âassociated X protein (Bax) and caspaseâ9 and increased apoptotic rate, and reduced expression levels of OSMR, Akt, phosphorylated (pâ)Akt, glycogen synthase kinaseâ3 (GSKâ3β), pâGSKâ3β, Bclâ2, insulinâlike growth factor 1 (IGFâ1), mammalian target of rapamycin (mTOR) and pâmTOR. The miRâ183 inhibitor decreased the expression levels of miRâ183, Bax and caspaseâ9 and the apoptotic rate; however, increased the expression of OSMR, Akt, pâAkt, GSKâ3β, pâGSKâ3β, Bclâ2, IGFâ1, mTOR and pâmTOR. The results of the present study provide evidence that the overexpression of miRâ183 promotes the apoptosis of substantia nigra neurons by inhibiting the expression of OSMR.
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