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Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway
Alzheimer’s disease (AD) is a progressive neurodegenerative disease. Evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue in the substantia nigra, blue plaque, and paraventricular nucleus. In this study, we investigated the effects of neural ste...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PAGEPress Publications, Pavia, Italy
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388643/ https://www.ncbi.nlm.nih.gov/pubmed/32705859 http://dx.doi.org/10.4081/ejh.2020.3135 |
Sumario: | Alzheimer’s disease (AD) is a progressive neurodegenerative disease. Evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue in the substantia nigra, blue plaque, and paraventricular nucleus. In this study, we investigated the effects of neural stem cell conditioned medium on the PCMT1/MST1 pathway to alleviate damage caused by amyloid β (Aβ)(25-35) in SH-SY5Y cells. Results demonstrated that Aβ(25-35) significantly decreased cell viability in both a time and dose-dependent manner. Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had an inhibitory effect on toxicity when fibrillation of Aβ(25-35) occurred, with a greater effect observed with NSC-CDM. An increase in PCMT1 expression levels was observed in the Aβ(25-35) + NSC-CDM group. sh-PCMT1 significantly reduced cell viability and inhibited the protective effects of NSC-CDM through the induction of apoptosis and increased expression of p- MST1. Overexpression of PCMT1 reversed the decrease in cell viability and apoptosis induced by Aβ(25-35). In summary, our findings suggest that NSC-CDM corrects the damage of Aβ(25-35) to cells by increasing levels of PCMT1, which in turn reduces phosphorylation of MST. |
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