ArticleInternational journal of molecular medicine2018
MicroRNA‑214 suppresses propofol‑induced neuroapoptosis through activation of phosphoinositide 3‑kinase/protein kinase B signaling by targeting phosphatase and tensin homolog expression.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- miR-29 as diagnostic biomarkers for tuberculosis: a systematic review and meta-analysis.Frontiers in public health · 2024Pooled it
- MicroRNA-339-5p inhibits lipopolysaccharide-induced rat mesangial cells by regulating the Syk/Ras/c-Fos pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Recent progress on the role of non-coding RNA in postoperative cognitive dysfunction.Frontiers in cellular neuroscience · 2022Review
- Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181aFrontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effects of microRNA (miR)‑214 on neuroapoptosis induced by propofol and the possible mechanism of its anti‑apoptotic effects. Initially, it was observed that miR‑214 expression was upregulated in propofol‑induced neuroapoptosis rats. Next, propofol‑treated nerve cells were transfected with miR‑214 mimics. The results revealed that miR‑214 overexpression induced apoptosis, inhibited cell proliferation, inhibited cyclin D1 protein expression, promoted caspase‑3 activity and B‑cell lymphoma 2‑associated X protein expression, and enhanced the levels of inflammation factors in nerve cells treated with propofol. In addition, miR‑214 overexpression suppressed phosphoinositide 3‑kinase/protein kinase B (PI3K/Akt) signaling by targeting the activation of phosphatase and tensin homolog (PTEN) and nuclear factor‑κB expression in nerve cells treated with propofol. Treatment with a PTEN inhibitor successfully suppressed the PTEN protein expression and decreased the apoptosis of propofol‑treated nerve cells subsequent to miR‑214 overexpression through PI3K/Akt signaling. In conclusion, the present study data revealed that miR‑214 suppressed propofol‑induced neuroapoptosis through the activation of PI3K/Akt signaling by targeting PTEN expression.
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