ArticleMolecular medicine (Cambridge, Mass.)2021
PIAS3 suppresses damage in an Alzheimer's disease cell model by inducing the STAT3-associated STAT3/Nestin/Nrf2/HO-1 pathway.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 16 citations in OpenAlex.
- Molecular Mechanisms of Indoor Environmental Pollution tt-DDE-Induced Blood Pressure Elevation and the Protective Role of Human-Specific Gene CHRFAM7A.Environment & health (Washington, D.C.) · 2026Article
- The therapeutic potential of neuroglobin-overexpressing human neural stem cells in a photothrombosis model.Regenerative therapy · 2025Article
- CPEB3 can regulate seizure susceptibility by inhibiting the transcriptional activity of STAT3 on NMDARs expression.Molecular medicine (Cambridge, Mass.) · 2025Article
- CARD9 protein SUMOylation regulates HOXB5 nuclear translocation and Parkin-mediated mitophagy in myocardial I/R injury.Journal of cellular and molecular medicine · 2024Article
- Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning.Molecular neurobiology · 2024Article
- Article
- SHP-1 alleviates atrial fibrosis in atrial fibrillation by modulating STAT3 activation.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Biomarker Genes Discovery of Alzheimer's Disease by Multi-Omics-Based Gene Regulatory Network Construction of Microglia.Brain sciences · 2022Article
- Renieramycin T Inhibits Melanoma B16F10 Cell Metastasis and Invasion via Regulating Nrf2 and STAT3 Signaling Pathways.Molecules (Basel, Switzerland) · 2022Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundAlzheimer'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.
methodsCerebrospinal 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.
resultsThe 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.
conclusionsSTAT3 reactivation by colivelin treatment negated the influence of PIAS3 on the survival, growth, apoptosis, and oxidative stress of Aβ-treated SH-SY5Y cells.
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