HucMSC extracellular vesicles increasing SATB 1 to activate the Wnt/β-catenin pathway in 6-OHDA-induced Parkinson's disease model.

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
IUBMB Life Pub Date : 2024-07-31 DOI:10.1002/iub.2893
Ying He, Ruicheng Li, Yuxi Yu, Zhiran Xu, Jiaxin Gao, Cancan Wang, Chushen Huang, Zhongquan Qi
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引用次数: 0

Abstract

Parkinson's disease (PD) is a degenerative disorder of the nervous system characterized by the loss of dopaminergic neurons and damage of neurons in the substantia nigra (SN) and striatum, resulting in impaired motor functions. This study aims to investigate how extracellular vesicles (EVs) derived from human umbilical cord mesenchymal stem cells (HucMSC) regulate Special AT-rich sequence-binding protein-1 (SATB 1) and influence Wnt/β-catenin pathway and autophagy in PD model. The PD model was induced by damaging SH-SY5Y cells and mice using 6-OHDA. According to the study, administering EVs every other day for 14 days improved the motor behavior of 6-OHDA-induced PD mice and reduced neuronal damage, including dopaminergic neurons. Treatment with EVs for 12 hours increased the viability of 6-OHDA-induced SH-SY5Y cells. The upregulation of SATB 1 expression with EV treatment resulted in the activation of the Wnt/β-catenin pathway in PD model and led to overexpression of β-catenin. Meanwhile, the expression of LC3 II was decreased, indicating alterations in autophagy. In conclusion, EVs could mitigate neuronal damage in the 6-OHDA-induced PD model by upregulating SATB 1 and activating Wnt/β-catenin pathway while also regulating autophagy. Further studies on the potential therapeutic applications of EVs for PD could offer new insights and strategies.

在 6-OHDA 诱导的帕金森病模型中,HucMSC 细胞外囊泡增加 SATB 1 以激活 Wnt/β-catenin 通路。
帕金森病(Parkinson's disease,PD)是一种神经系统退行性疾病,其特征是黑质(SN)和纹状体中多巴胺能神经元的缺失和损伤,从而导致运动功能受损。本研究旨在探讨人脐带间充质干细胞(HucMSC)提取的细胞外囊泡(EVs)如何调控特殊富AT序列结合蛋白-1(SATB 1),以及如何影响PD模型中的Wnt/β-catenin通路和自噬。PD模型是通过使用6-OHDA损伤SH-SY5Y细胞和小鼠而诱发的。研究发现,连续14天隔天服用EVs可改善6-OHDA诱导的帕金森病小鼠的运动行为,并减少神经元损伤,包括多巴胺能神经元。用EVs治疗12小时可提高6-OHDA诱导的SH-SY5Y细胞的活力。EV 处理可上调 SATB 1 的表达,从而激活 PD 模型中的 Wnt/β-catenin 通路,并导致 β-catenin 的过度表达。同时,LC3 II的表达减少,表明自噬发生了改变。总之,在6-OHDA诱导的帕金森病模型中,EVs可通过上调SATB 1和激活Wnt/β-catenin通路减轻神经元损伤,同时还能调节自噬。对EVs治疗帕金森病的潜在应用的进一步研究可提供新的见解和策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
IUBMB Life
IUBMB Life 生物-生化与分子生物学
CiteScore
10.60
自引率
0.00%
发文量
109
审稿时长
4-8 weeks
期刊介绍: IUBMB Life is the flagship journal of the International Union of Biochemistry and Molecular Biology and is devoted to the rapid publication of the most novel and significant original research articles, reviews, and hypotheses in the broadly defined fields of biochemistry, molecular biology, cell biology, and molecular medicine.
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