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SETD5-AS1 stimulates neuron death in stroke via promoting PTEN expression
1Department of Neurology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, China. 13780891068@163.com.
European Review for Medical and Pharmacological Sciences
|October 4, 2018
Summary
Long non-coding RNA SETD5-AS1 is highly expressed in ischemic stroke models. It promotes stroke by activating PTEN and inhibiting the PI3K/AKT pathway, contributing to cell injury.
Area of Science:
- Molecular Biology
- Neuroscience
- Genetics
Background:
- Ischemic stroke is a leading cause of death and disability worldwide.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in various biological processes, including neurological diseases.
- The specific function of lncRNA SETD5-AS1 in ischemic stroke remains largely unexplored.
Purpose of the Study:
- To elucidate the role of lncRNA SETD5-AS1 in the pathogenesis of ischemic stroke.
- To investigate the underlying molecular mechanisms by which SETD5-AS1 influences ischemia-reperfusion injury.
Main Methods:
- Establishment of middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation/reoxygenation (OGD/R) models in mice and cells.
- Quantitative Real-time-polymerase chain reaction (qRT-PCR) to assess SETD5-AS1 expression.
- Cell proliferation and apoptosis assays following SETD5-AS1 manipulation.
- Dual-luciferase reporter, RNA pull-down, and RNA immunoprecipitation (RIP) assays to determine gene interactions.
- Western blot analysis to evaluate pathway activation.
Main Results:
- SETD5-AS1 expression was significantly upregulated in ischemia-reperfusion injury models.
- Overexpression of SETD5-AS1 led to increased N2a cell apoptosis and decreased proliferation.
- PTEN (Phosphatase and tensin homolog) expression was upregulated, and SETD5-AS1 was found to promote PTEN transcription.
- SETD5-AS1 was confirmed to directly bind with PTEN.
- SETD5-AS1 overexpression inhibited the PI3K/AKT signaling pathway.
Conclusions:
- SETD5-AS1 is highly expressed in ischemic stroke models, indicating its involvement in the disease.
- SETD5-AS1 exacerbates ischemia-reperfusion injury by upregulating PTEN and consequently inhibiting the PI3K/AKT pathway.
- Targeting SETD5-AS1 may offer a potential therapeutic strategy for ischemic stroke.
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