Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion

Autor:	Xunran Ni, Wenbo Xia, Guozhong Li, Yanli Zhang, Zhiqiang Su, Kejuan Jia, Qian Su
Jazyk:	angličtina
Rok vydání:	2020
Předmět:	STAT3 Transcription Factor Immunology lcsh:Medicine Apoptosis Diseases Article Brain Ischemia Drug Delivery Systems Downregulation and upregulation medicine Humans Viability assay STAT3 lcsh:Science Protein kinase B Cells Cultured Inflammation Neurons Gene knockdown Multidisciplinary biology Microglia business.industry lcsh:R Cell Polarity Flow Cytometry Up-Regulation Blot Oxygen medicine.anatomical_structure Glucose Neurology Cancer research biology.protein RNA Long Noncoding lcsh:Q business Proto-Oncogene Proteins c-akt Signal Transduction Neuroscience
Zdroj:	Scientific Reports, Vol 10, Iss 1, Pp 1-9 (2020) Scientific Reports
ISSN:	2045-2322
Popis:	Acute cerebral ischaemia may lead to serious consequences, including brain injury caused by uncontrolled reperfusion, which occurs when circulation is re-established. The long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) plays an important role in the immune system. However, the potential roles and underlying molecular mechanisms of NEAT1 in cerebral ischaemia/reperfusion (I/R) injury remain unclear. The aim of the present study was to investigate the function of the lncRNA NEAT1 in cerebral I/R injury and its potential beneficial effects on neurons. In our study, oxygen–glucose deprivation (OGD)/reoxygenation (OGD/R) was induced in vitro to mimic cerebral I/R injury. Cholecystokinin-octopeptide (CCK-8) was used to measure cell viability, and flow cytometry was used to measure cell apoptosis. Real-time quantitative PCR (qRT-PCR) was used to measure the expression of phenotypic markers of classically activated (M1) and alternatively activated (M2) microglia, and western blotting was performed to detect the levels of proteins related to the AKT/STAT3 pathway. The expression of the lncRNA NEAT1 was significantly upregulated in patients with ischaemic stroke, and knockdown of the lncRNA NEAT1 alleviated OGD/R-induced apoptosis and increased neuronal viability. Furthermore, the lncRNA NEAT1 may inhibit microglial polarization towards the M1 phenotype to reduce the damage caused by OGD/R and reduce the activity of the AKT/STAT3 pathway. In conclusion, the lncRNA NEAT1 may be a potential target for new therapeutic interventions for cerebral I/R.
Databáze:	OpenAIRE
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