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Upregulation of miR-376c-3p alleviates oxygen–glucose deprivation-induced cell injury by targeting ING5
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Upregulation of miR-376c-3p alleviates oxygen–glucose deprivation-induced cell injury by targeting ING5
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Upregulation of miR-376c-3p alleviates oxygen–glucose deprivation-induced cell injury by targeting ING5
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Journal Article
Upregulation of miR-376c-3p alleviates oxygen–glucose deprivation-induced cell injury by targeting ING5
2019
Overview
Background
The expression level of miR-376c-3p is significantly lower in infants with neonatal hypoxic-ischemic encephalopathy (HIE) than in healthy infants. However, the biological function of this microRNA remains largely elusive.
Methods
We used PC-12 and SH-SY5Y cells to establish an oxygen–glucose deprivation (OGD) cell injury model to mimic HIE in vitro. The miR-376c-3p expression levels were measured using quantitative reverse transcription PCR. The CCK-8 assay and flow cytometry were utilized to evaluate OGD-induced cell injury. The association between miR-376c-3p and inhibitor of growth 5 (ING5) was validated using the luciferase reporter assay. Western blotting was conducted to determine the protein expression of CDK4, cyclin D1, Bcl-2 and Bax.
Results
MiR-376c-3p was significantly downregulated in the OGD-induced cell injury model. Its overexpression elevated cell viability and impaired cell cycle G0/G1 phase arrest and apoptosis in PC-12 and SH-SY5Y cells after OGD. Downregulation of miR-376c-3p gave the opposite results. We further demonstrated that ING5 was a negatively regulated target gene of miR-376c-3p. Importantly, ING5 knockdown had a similar effect to miR-376c-3p-mediated protective effects against cell injury induced by OGD. Its overexpression abolished these protective effects.
Conclusion
Our data suggest that miR-376c-3p downregulated ING5 to exert protective effects against OGD-induced cell injury in PC-12 and SH-SY5Y cells. This might represent a novel therapeutic approach for neonatal HIE treatment.
Publisher
BioMed Central,Springer Nature B.V,BMC
Subject
/ bcl-2-Associated X Protein - genetics
/ bcl-2-Associated X Protein - metabolism
/ Biological and Medical Physics
/ Biomedical and Life Sciences
/ Cell Survival - drug effects
/ Cyclin-Dependent Kinase 4 - genetics
/ Cyclin-Dependent Kinase 4 - metabolism
/ G1 phase
/ Glucose
/ Humans
/ Hypoxia
/ Infants
/ ING5
/ Ischemia
/ miRNA
/ Neonates
/ Proteins
/ Proto-Oncogene Proteins c-bcl-2 - genetics
/ Proto-Oncogene Proteins c-bcl-2 - metabolism
/ Rats
/ Software
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumor Suppressor Proteins - genetics
