MicroRNA-146a inhibition promotes total neurite outgrowth and suppresses cell apoptosis, inflammation, and STAT1/MYC pathway in PC12 and cortical neuron cellular Alzheimer's disease models
Autor: | Ma, Yinghui, Ye, Jiye, Zhao, Li, Pan, Dongmei |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Medicine (General) Neurite QH301-705.5 Physiology Neuronal Outgrowth Immunology Biophysics Apoptosis Ocean Engineering Inflammation PC12 Cells Biochemistry Proinflammatory cytokine 03 medical and health sciences Total neurite outgrowth R5-920 0302 clinical medicine Alzheimer Disease medicine Animals Biology (General) General Pharmacology Toxicology and Pharmaceutics Neurons Chemistry General Neuroscience MicroRNA 146a STAT1/MYC Interleukin Cell Biology General Medicine Transfection Alzheimer's disease Rats Cell biology MicroRNAs STAT1 Transcription Factor 030104 developmental biology Nerve growth factor 030220 oncology & carcinogenesis Cell apoptosis Tumor necrosis factor alpha medicine.symptom Research Article |
Zdroj: | Brazilian Journal of Medical and Biological Research v.54 n.5 2021 Brazilian Journal of Medical and Biological Research Associação Brasileira de Divulgação Científica (ABDC) instacron:ABDC Brazilian Journal of Medical and Biological Research, Vol 54, Iss 5 (2021) |
Popis: | This study aimed to explore the effect of microRNA (miR)-146a inhibition on regulating cell apoptosis, total neurite outgrowth, inflammation, and STAT1/MYC pathway in Alzheimer's disease (AD). PC12 and cortical neuron cellular AD models were constructed by Aβ1-42 insult. For the former model, nerve growth factor (NGF) stimulation was previously conducted. miR-146a inhibitor and negative-control (NC) inhibitor were transfected into the two cellular AD models, and then cells were named miR-inhibitor group and NC-inhibitor group, respectively. After transfection, cell apoptosis, total neurite outgrowth, supernatant inflammation cytokines, and STAT1/MYC pathway were detected. miR-146a expression was similar between PC12 cellular AD model and control cells (NGF-stimulated PC12 cells), while miR-146a expression was increased in cortical neuron cellular AD model compared with control cells (rat embryo primary cortical neurons). In both PC12 and cortical neuron cellular AD models, miR-146a expression was reduced in miR-inhibitor group compared with NC-inhibitor group after transfection. Furthermore, cell apoptosis was attenuated, while total neurite outgrowth was elevated in miR-inhibitor group compared with NC-inhibitor group. As for supernatant inflammatory cytokines, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-17 levels were lower in miR-inhibitor group than in NC-inhibitor group. Additionally, STAT1 and c-Myc mRNA and protein expressions were attenuated in miR-inhibitor group compared with NC-inhibitor group. In conclusion, miR-146a potentially represented a viable therapeutic target for AD. |
Databáze: | OpenAIRE |
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