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Objective <p>This study aimed to investigate how circ-find-0001774 regulates miR-153-3p in Parkinson’s disease (PD).</p> Methods <p>We first validated the targeting relationship between circ-find-0001774 and miR-153-3p using dual-luciferase reporter assays, excluding any association with let-7a-5p. Next, we constructed a circ-find-0001774 overexpression vector and transfected it into MN9D dopaminergic neurons, confirming transfection efficiency by qPCR. In vitro, we induced a PD cell model with 100 µmol/L MPP+ iodide for 24&#xa0;h and assessed cell proliferation using CCK-8, apoptosis via flow cytometry, and miR-153-3p and LC3Ⅱ/Ⅰ protein levels by qPCR and Western blotting. In vivo, we established a mouse PD model by daily intraperitoneal injection of 18&#xa0;mg/kg MPTP for seven days, evaluating motor function through behavioral tests, observing brain pathology via HE staining, and analyzing miR-153-3p and β-catenin protein levels by qPCR and Western blotting.</p> Results <p>Dual-luciferase assays confirmed a specific targeting interaction between miR-153-3p and circ-find-0001774. In vitro, circ-find-0001774 overexpression significantly enhanced cell proliferation, reduced apoptosis and decreased miR-153-3p and LC3Ⅱ/Ⅰ protein expression levels. In vivo, circ-find-0001774 overexpression notably ameliorated motor deficits in the mouse PD model mitigated neurodegeneration, decreased miR-153-3p level and increased β-catenin protein expression levels.</p> Conclusion <p>Our study reveals that circ-find-0001774 modulates miR-153-3p, mainly through the Wnt/β-Catenin signaling pathway, suggesting its therapeutic potential for PD. These findings provide novel insights and experimental foundations for further developing PD treatment strategies.</p>

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Circ-find-0001774 Modulates Parkinson’s Disease via miR-153-3p: Mechanistic Insights and Therapeutic Implications

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月30日

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  • Ronglan Zhu,
  • Jie Chen,
  • Tao Song,
  • Yun Yang,
  • Chaoyang Zhou,
  • Zhiping Xie,
  • Min Yuan,
  • Jianzhong Zhang

摘要

Objective

This study aimed to investigate how circ-find-0001774 regulates miR-153-3p in Parkinson’s disease (PD).

Methods

We first validated the targeting relationship between circ-find-0001774 and miR-153-3p using dual-luciferase reporter assays, excluding any association with let-7a-5p. Next, we constructed a circ-find-0001774 overexpression vector and transfected it into MN9D dopaminergic neurons, confirming transfection efficiency by qPCR. In vitro, we induced a PD cell model with 100 µmol/L MPP+ iodide for 24 h and assessed cell proliferation using CCK-8, apoptosis via flow cytometry, and miR-153-3p and LC3Ⅱ/Ⅰ protein levels by qPCR and Western blotting. In vivo, we established a mouse PD model by daily intraperitoneal injection of 18 mg/kg MPTP for seven days, evaluating motor function through behavioral tests, observing brain pathology via HE staining, and analyzing miR-153-3p and β-catenin protein levels by qPCR and Western blotting.

Results

Dual-luciferase assays confirmed a specific targeting interaction between miR-153-3p and circ-find-0001774. In vitro, circ-find-0001774 overexpression significantly enhanced cell proliferation, reduced apoptosis and decreased miR-153-3p and LC3Ⅱ/Ⅰ protein expression levels. In vivo, circ-find-0001774 overexpression notably ameliorated motor deficits in the mouse PD model mitigated neurodegeneration, decreased miR-153-3p level and increased β-catenin protein expression levels.

Conclusion

Our study reveals that circ-find-0001774 modulates miR-153-3p, mainly through the Wnt/β-Catenin signaling pathway, suggesting its therapeutic potential for PD. These findings provide novel insights and experimental foundations for further developing PD treatment strategies.