Downregulation of miR‑21 suppresses 1‑methyl‑4‑phenylpyridinium‑induced neuronal damage
in MES23.5 cells
Affiliations: Department of Neurology, The Second People's Hospital of Taizhou, Taizhou, Jiangsu 225500, P.R. China
- Published online on: August 5, 2019 https://doi.org/10.3892/etm.2019.7853
Copyright: © Mao
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
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Accumulating evidence suggests that overproduction of oxidative stress, increases neuroinflammation and activates apoptosis. These two processes are associated with the development of Parkinson's disease (PD). The present study aimed to investigate the role of miR‑21 in the development of PD. 1‑Methyl‑4‑phenylpyridinium (MPP+) was used to induce a PD‑like model in MES23.5 cells. The results of the reverse transcription‑quantitative PCR assays indicated that miR‑21 levels were markedly increased in MES23.5 cells following MPP+ treatment. Furthermore, MES23.5 cells were transfected with miR‑21 inhibitor, mimics and/or relevant negative control, following MPP+ administration. The results of the functional assays revealed that downregulation of miR‑21 significantly attenuated the induction of cell apoptosis and reactive oxygen species (ROS) production, while it enhanced the survival of MPP+‑induced MES23.5 cells. Furthermore, downregulation of miR‑21 increased the expression levels of tyrosine hydroxylase, whereas suppression of miR‑21 inhibited the production of pro‑inflammatory cytokines [interleukin (IL)‑6, IL‑1β and tumor necrosis factor‑α] in MES23.5 cells. Western blot analysis further indicated that the Bcl‑2/Bax protein expression ratio was significantly increased and double luciferase assay analysis confirmed that Bcl‑2 was a direct target of miR‑21. Taken collectively, the data demonstrated that downregulation of miR‑21 protected cells from MPP+‑mediated cytotoxicity by the inhibition of apoptosis induction, the reduction of the inflammatory response and the suppression of ROS production. The present findings may provide novel approaches for PD clinical treatment.