PIAS3 suppresses damage in an Alzheimer’s disease cell model by inducing the STAT3-associated STAT3/Nestin/Nrf2/HO-1 pathway
| Autor: | Qiaoya Ma, Chen Li, Chunting Hu, Ruili Wang, Youyou Zhang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Oxidative
PIAS3 Apoptosis medicine.disease_cause Biochemistry STAT3 Nestin Medicine Genetics (clinical) Aβ Aged 80 and over biology Intracellular Signaling Peptides and Proteins Middle Aged Protein Inhibitors of Activated STAT medicine.anatomical_structure Molecular Medicine Alzheimer’s disease Research Article Signal Transduction Adult STAT3 Transcription Factor Amyloid beta Cell Survival NF-E2-Related Factor 2 Central nervous system RM1-950 QD415-436 Models Biological Young Adult Alzheimer Disease Cell Line Tumor Genetics Humans Molecular Biology Aged Amyloid beta-Peptides business.industry Molecular medicine biology.protein STAT protein Cancer research Therapeutics. Pharmacology business Reactive Oxygen Species Oxidative stress Heme Oxygenase-1 Molecular Chaperones |
| Zdroj: | Molecular Medicine Molecular Medicine, Vol 27, Iss 1, Pp 1-13 (2021) |
| ISSN: | 1528-3658 1076-1551 |
| Popis: | Background Alzheimer’s disease (AD), the most common form of dementia, is caused by the degeneration of the central nervous system (CNS). A previous study reported that signal transducer and activator of transcription 3 (STAT3) is activated during AD development; nonetheless, the related mechanism remains unknown. Thus, this study used a cell model to explore whether and how the protein inhibitor of activated STAT3 (PIAS3) is involved in AD development. Methods Cerebrospinal fluid (CSF) specimens of 30 patients with AD and 10 normal participants were included in this study. SH-SY5Y cells were used to constructed AD model. Relevant indices were then detected and analyzed. Results The results showed that compared with the control group, PIAS3 expression was substantially decreased in patients with AD and amyloid beta (Aβ)-treated SH-SY5Y cells. PIAS3 overexpression was able to reverse the detrimental effects of Aβ treatment on cell survival and growth. Further, it could also ameliorate apoptosis and oxidative stress in Aβ-treated SH-SY5Y cells. Additionally, PIAS3 was shown to reduce the activated form of STAT3 and increase the activity of the downstream Nestin/nuclear factor erythroid 2-related factor/heme oxygenase-1 pathway. Conclusions STAT3 reactivation by colivelin treatment negated the influence of PIAS3 on the survival, growth, apoptosis, and oxidative stress of Aβ-treated SH-SY5Y cells. |
| Databáze: | OpenAIRE |
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