Open Access

ARTICLE

Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SH-SY5Y cells induced by Aβ_25-35

by XINWEI WU¹, GUOYONG JIA^2,*, HONGNA YANG³, CONGCONG SUN², YING LIU², ZENGYAN DIAO²

1 Department of Geriatrics, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China
2 Department of Neurology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China
3 Department of Critical-Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China

* Corresponding Author:GUOYONG JIA,

BIOCELL 2022, 46(2), 471-478. https://doi.org/10.32604/biocell.2021.015701

Received 07 January 2021; Accepted 22 March 2021; Issue published 20 October 2021

Abstract

A progressive neurodegenerative disease, Alzheimer’s disease (AD). Studies suggest that highly expressed protein isoaspartate methyltransferase 1 (PCMT1) in brain tissue. In the current study, we explored the effects of neural stem cell-conditioned medium (NSC-CDM) on the PCMT1/MST1 pathway to alleviate Aβ_25-35-induced damage in SH-SY5Y cells. Our data suggested that Aβ25-35 markedly inhibited cell viability. NSC-CDM or Neural stem cell-complete medium (NSC-CPM) had a suppression effect on toxicity when treatment with Aβ_25-35, with a greater effect observed with NSC-CDM. Aβ_25-35 + NSC-CDM group exhibited an increase in PCMT1 expression. sh-PCMT1 markedly decreased cell proliferation and suppressed the protective role of NSC-CDM through the induction of apoptosis and improved p-MST1 expression. Overexpression of PCMT1 reversed the Aβ_25-35-induced decrease in cell proliferation and apoptosis. In summary, our findings suggest that NSC-CDM corrects the Aβ_25-35- induced damage to cells by improving PCMT1 expressions, which in turn reduces phosphorylation of MST1.

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