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MicroRNA-361-3p Regulates Autophagy and Apoptotic Processes by Regulating PI3K/Akt Signaling in Parkinson's Disease

Pingting Chen1, Jing Yang2, Yixuan Xu2

  • 1Department of Neurology, Wenling TCM Hospital Affiliated to Zhejiang Chinese Medical University, Taizhou, 317500, China.

Neurochemical Research
|June 30, 2025
PubMed

Insights

MicroRNA-361-3p protects against Parkinson's disease (PD) by reducing cell death and apoptosis. Upregulating this microRNA inhibits PD progression by targeting PFKFB3 and activating the PI3K/Akt pathway.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) play a crucial role in the pathogenesis of Parkinson's disease (PD).
  • Understanding the specific roles of miRNAs in PD is essential for developing targeted therapies.
  • Dysregulation of cellular processes like apoptosis and autophagy is implicated in PD.

Purpose of the Study:

  • To investigate the effect of microRNA (miR)-361-3p on apoptosis and autophagy in a Parkinson's disease (PD) cell model.
  • To elucidate the underlying molecular mechanisms of miR-361-3p in PD pathogenesis.
  • To explore the potential of miR-361-3p as a therapeutic target for PD.

Main Methods:

  • Established an in vitro Parkinson's disease (PD) cell model using SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium ion (MPP+).
  • Manipulated miR-361-3p expression via cell transfection and assessed cell viability (CCK-8), apoptosis (flow cytometry), and inflammatory factors (ELISA).
  • Analyzed autophagy-associated proteins (Beclin 1, LC3) and PI3K/Akt signaling pathway proteins (p-PI3K, p-Akt) using Western blot; verified miR-361-3p target gene (PFKFB3) interaction via luciferase reporter assay.

Main Results:

  • MPP+ treatment decreased miR-361-3p expression and cell viability in a dose-dependent manner.
  • Overexpression of miR-361-3p significantly enhanced cell survival, reduced apoptosis, and modulated autophagy proteins (decreased Beclin 1, LC3II/LC3I ratio) in MPP+-induced cells.
  • miR-361-3p upregulation inhibited PFKFB3 expression, and subsequent PFKFB3 overexpression reversed the protective effects of miR-361-3p, while activating the PI3K/Akt pathway.

Conclusions:

  • miR-361-3p expression is reduced in Parkinson's disease (PD) cell models.
  • Overexpression of miR-361-3p exerts neuroprotective effects by inhibiting apoptosis and modulating autophagy.
  • miR-361-3p functions via regulating PFKFB3 and activating the PI3K/Akt signaling pathway, offering a potential therapeutic strategy for PD.
Keywords:
AutophagyMiR-361-3pPI3K/AktParkinson’s disease

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