Abstract |
Ischemic stroke is characterized by loss of brain function because of cerebral ischemia. Evidence has been shown that miR-217-5p is significantly downregulated in infarcted brain areas following focal cerebral ischemia. However, the role of miR-217-5p in ischemic stroke is still unclear. To mimic ischemia/reperfusion (I/R) injury conditions in vitro, SH-SY5Y cells were treated with oxygen- glucose deprivation/reperfusion (OGD/R). Our data found that PTEN was the directly target of miR-217-5p in SH-SY5Y cells. The level of miR-217-5p was significantly decreased, while the level of PTEN was notably increased in SH-SY5Y cells following OGD/R treatment. Overexpression of miR-217-5p markedly promoted the proliferation and cell cycle progression, and inhibited apoptosis in OGD/R-treated SH-SY5Y cells. In addition, overexpression of miR-217-5p significantly decreased the expressions of PTEN and FOXO1, but increased the expression of p-Akt in OGD/R-treated SH-SY5Y cells. Moreover, methylation specific PCR (MSP) results indicated the CpG islands in the promoter region of miR-217-5p were hypermethylated in SH-SY5Y cells under OGD/R. Meanwhile, the DNA methylation of miR-217-5p promoter region decreased expression of miR-217-5p. Our data indicated that miR-217-5p could attenuate ischemic injury by inhibiting PTEN. In addition, DNA methylation-mediated silencing of miR-217-5p may serve as a promising therapeutic target of ischemic stroke.
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Authors | Zhongquan Yi, Yuanyuan Shi, Panwen Zhao, Yun Xu, Pinglei Pan |
Journal | Human cell
(Hum Cell)
Vol. 33
Issue 4
Pg. 1026-1035
(Oct 2020)
ISSN: 1749-0774 [Electronic] Japan |
PMID | 32683553
(Publication Type: Journal Article)
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Chemical References |
- MIRN217 microRNA, human
- MicroRNAs
- PTEN Phosphohydrolase
- PTEN protein, human
- Glucose
- Oxygen
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Topics |
- Cells, Cultured
- DNA Methylation
- Gene Expression
(genetics)
- Glucose
(metabolism)
- Humans
- MicroRNAs
(genetics, metabolism, physiology)
- Molecular Targeted Therapy
- Neurons
(pathology)
- Oxygen
(metabolism)
- PTEN Phosphohydrolase
(genetics, metabolism)
- Reperfusion Injury
(etiology, genetics, therapy)
- Up-Regulation
(genetics)
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