Open Access

Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease

  • Authors:
    • Jin-Xia Gao
    • Yu Li
    • Sai-Nan Wang
    • Xing-Chi Chen
    • Lu-Lu Lin
    • Hui Zhang
  • View Affiliations

  • Published online on: November 7, 2018     https://doi.org/10.3892/ijmm.2018.3982
  • Pages: 209-220
  • Copyright: © Gao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to investigate the effect of microRNA‑183 (miR‑183) 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 transferase‑mediated dUTP‑biotin nick end‑labeling, respectively. Substantia nigra neurons in normal and PD mice were cultured in vitro. The association between miR‑183 and OSMR was verified using a dual luciferase reporter gene assay. The expression of miR‑183 and the phosphoinositide 3‑kinase‑Akt signaling pathway‑associated genes were detected by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. Cell apoptosis was detected by flow cytometry. OSMR is the target gene of miR‑183. The number of OSMR‑positive cells and the apoptotic rate of substantia nigra neurons were increased in the PD group. Neurons transfected with miR‑183 mimic exhibited elevated expression levels of miR‑183, B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax) and caspase‑9 and increased apoptotic rate, and reduced expression levels of OSMR, Akt, phosphorylated (p‑)Akt, glycogen synthase kinase‑3 (GSK‑3β), p‑GSK‑3β, Bcl‑2, insulin‑like growth factor 1 (IGF‑1), mammalian target of rapamycin (mTOR) and p‑mTOR. The miR‑183 inhibitor decreased the expression levels of miR‑183, Bax and caspase‑9 and the apoptotic rate; however, increased the expression of OSMR, Akt, p‑Akt, GSK‑3β, p‑GSK‑3β, Bcl‑2, IGF‑1, mTOR and p‑mTOR. The results of the present study provide evidence that the overexpression of miR‑183 promotes the apoptosis of substantia nigra neurons by inhibiting the expression of OSMR.
View Figures
View References

Related Articles

Journal Cover

January 2019
Volume 43 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
APA
Gao, J., Li, Y., Wang, S., Chen, X., Lin, L., & Zhang, H. (2019). Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease. International Journal of Molecular Medicine, 43, 209-220. https://doi.org/10.3892/ijmm.2018.3982
MLA
Gao, J., Li, Y., Wang, S., Chen, X., Lin, L., Zhang, H."Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease". International Journal of Molecular Medicine 43.1 (2019): 209-220.
Chicago
Gao, J., Li, Y., Wang, S., Chen, X., Lin, L., Zhang, H."Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease". International Journal of Molecular Medicine 43, no. 1 (2019): 209-220. https://doi.org/10.3892/ijmm.2018.3982