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Updated: Apr 22, 2026
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells
Jie Qiu1, Xiao-Yu Zhou2, Xiao-Guang Zhou2
1Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China.
Abstract:
It was previously demonstrated that microRNA-210 (miR-210) exhibited neuroprotective effects in a murine model of hypoxic-ischemic encephalopathy via inhibition of apoptosis. The aim of the present study was to further elucidate the effect of miR-210 on apoptosis in PC12 cells following transfection with miR-210 inhibitors and exposure to oxygen glucose deprivation (OGD). The expression levels of miR-210 were identified using reverse transcription-quantitative polymerase chain reaction analysis. Apoptosis was investigated using Annexin V-fluorescein isothiocyanate assays. Apoptosis-related protein expression levels were studied with western blot analysis. The results showed that the expression levels of miR-210 were upregulated in PC12 cells following a 4-h exposure to OGD, relative to those in normoxic control cells. miR-210 knockdown increased cell apoptosis by inducing caspase activity and regulating the balance between Bcl-2 and Bax levels. The present study demonstrated that miR-210 knockdown induced cell apoptosis using an ex vivo model of ischemic hypoxia (IH). Knockdown of miR-210 represents a potential novel therapeutic approach to combat neonatal IH.
Insights
MicroRNA-210 (miR-210) plays a key role in protecting against hypoxic-ischemic encephalopathy. Inhibiting miR-210 in cells exposed to oxygen glucose deprivation (OGD) increases apoptosis, suggesting a therapeutic target for neonatal ischemic hypoxia.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- MicroRNA-210 (miR-210) has demonstrated neuroprotective properties in models of hypoxic-ischemic encephalopathy by inhibiting apoptosis.
- The precise role of miR-210 in cellular apoptosis under ischemic conditions requires further investigation.
Purpose of the Study:
- To investigate the effect of miR-210 inhibition on apoptosis in PC12 cells subjected to oxygen glucose deprivation (OGD).
- To explore the molecular mechanisms underlying miR-210's influence on apoptosis.
Main Methods:
- PC12 cells were transfected with miR-210 inhibitors and exposed to OGD.
- miR-210 expression was quantified using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).
- Apoptosis was assessed via Annexin V-fluorescein isothiocyanate (FITC) assays and western blot analysis of apoptosis-related proteins (caspase activity, Bcl-2, Bax).
Main Results:
- miR-210 expression was significantly upregulated in PC12 cells after 4-hour OGD exposure compared to normoxic controls.
- Knockdown of miR-210 led to increased cell apoptosis.
- miR-210 inhibition induced apoptosis by activating caspase activity and altering the Bcl-2/Bax protein ratio.
Conclusions:
- miR-210 knockdown exacerbates apoptosis in an ex vivo model of ischemic hypoxia (IH).
- Targeting miR-210 may offer a novel therapeutic strategy for neonatal IH.
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