Olfactory mucosal mesenchymal stem cell-derived exosome Lnc A2M-AS1 ameliorates oxidative stress by regulating TP53INP1-mediated mitochondrial autophagy through interacting with IGF2BP1 in Parkinson's diseases

被引:0
作者
Zhang, Jiangshan [1 ]
Wang, Chuang [2 ]
Yang, Guoshuai [1 ]
Zhou, Yanhui [1 ]
Hou, Dan [1 ]
Xia, Ying [2 ]
机构
[1] Cent South Univ, Affiliated Haikou Hosp, Xiangya Sch Med, Dept Neurol, Haikou 570208, Hainan, Peoples R China
[2] Cent South Univ, Affiliated Haikou Hosp, Xiangya Sch Med, Dept Neurosurg, 43 Renmin Ave, Haikou 570208, Hainan, Peoples R China
关键词
Parkinson's Disease; Olfactory Mucosa Mesenchymal Stem Cell; Exosome; Mitophagy; Oxidative Stress; Lnc A2M-AS1; MITOPHAGY;
D O I
10.1007/s10565-025-10009-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
BackgroundExosome Lnc A2M-AS1 from olfactory mucosa mesenchymal stem cells (OM-MSCs) can ameliorate oxidative stress by improving mitophagy in cardiomuscular cells; however, it remains unclear whether this effect exists in the brain tissues of patients with Parkinson's disease (PD).MethodsOM-MSC-Exosomes were isolated and verified based on morphology and specific biomarkers. The effects of OM-MSC-Exo on mitochondrial autophagy, oxidative stress, and lncRNA A2M-AS1 were detected in MPP+-treated HT22 cells. The effects of OM-MSC-Exos on mitochondrial autophagy and oxidative stress were detected in an MPTP-induced Parkinson's disease (PD) model in C57BL/6 mice. The interaction between IGF2BP1, A2M-AS1, and TP53INP1 was assessed via RNA pull-down/RNA Immunoprecipitation and RNA stability assays. The effects of lnc A2M-AS1 on IGF2BP1/TP53INP1-mediated mitochondrial autophagy and oxidative stress were verified in MPP+-treated HT22 cells and MPTP-induced PD mouse models.ResultsExosomes isolated from olfactory mucosa mesenchymal stem cells were found to be rich in Lnc A2M-AS1. Lnc A2M-AS1 was proved to be able to ameliorate oxidative stress induced by MPP+ in HT22 cells. lncRNA A2M-AS1 regulates oxidative stress by enhancing mitophagy in HT22 cells. In addition, lncRNA A2M-AS1 induced mitophagy through TP53INP1 and mediated TP53INP1 expression by binding to IGF2BP1. Furthermore, OM-MSC-Exo and Lnc A2M-AS1 treatment improved symptoms and ameliorated oxidative stress in MPTP-induced PD mouse models.ConclusionCollectively, lncRNA A2M-AS1 from OM-MSC-derived exosomes regulates TP53INP1 expression by targeting IGF2BP1 to induce mitophagy and ameliorate oxidative stress. OM-MSC-derived exosomes could potentially serve as promising candidates for new treatment methods for PD.
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页数:19
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