ArticleCNS neuroscience & therapeutics2012
Basic fibroblast growth factor protects C17.2 cells from radiation-induced injury through ERK1/2.
Article in CNS neuroscience & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Phenotypic risk factors linked to acute radiation-induced toxicities: a phenome-wide Mendelian randomization study of 12,042 cancer patients.Journal of Cancer · 2026Article
- Advance and Prospect of Positron Emission Tomography in Alzheimer's disease research.Molecular psychiatry · 2025Review
- Article
- Curcumin inhibits oxidative stress and autophagy in C17.2 neural stem cell through ERK1/2 signaling pathways.Aging medicine (Milton (N.S.W)) · 2024Article
- Dual Specificity Phosphatase 6 Protects Neural Stem Cells from β-Amyloid-Induced Cytotoxicity through ERK1/2 Inactivation.Biomolecules · 2018Article
- Once the Light Touch to the Brain: Cytotoxic Effects of Low-Dose Gamma-Ray, Laser Light, and Visible Light on Rat Neuronal Cell Culture.The Eurasian journal of medicine · 2016Article
- PI3K/Akt/FoxO3a signaling mediates cardioprotection of FGF-2 against hydrogen peroxide-induced apoptosis in H9c2 cells.Molecular and cellular biochemistry · 2016Article
- A kinome-targeted RNAi-based screen links FGF signaling to H2AX phosphorylation in response to radiation.Cellular and molecular life sciences : CMLS · 2015Article
- The antiaging activity and cerebral protection of rapamycin at micro-doses.CNS neuroscience & therapeutics · 2014Article
- Toll-like receptor 4-mediated signaling participates in apoptosis of hippocampal neurons.Neural regeneration research · 2013Article
- Edaravone protects HT22 neurons from H2O2-induced apoptosis by inhibiting the MAPK signaling pathway.CNS neuroscience & therapeutics · 2013Article
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8 authors.
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Abstract
aimsTo establish a radiation-induced neural injury model using C17.2 neural stem cells (NSCs) and to investigate whether basic fibroblast growth factor (bFGF) can protect the radiation-induced injury of C17.2 NSCs. Furthermore, we aim to identify the possible mechanisms involved in this model.
methodsC17.2 NSCs received a single exposure (3, 6, and 9 Gy, respectively) at a dose rate of 300 cGy/min with a control group receiving 0 Gy. Different concentrations of bFGF were added for 24 h, 5 min postirradiation. The MTS assay and flow cytometry were used to detect cytotoxicity and apoptosis. Expression of FGFR1, ERK1/2, and p-ERK1/2 proteins was detected with or without U0126 was pretreated prior to C17.2 NSCs receiving irradiation.
resultsC17.2 NSCs showed a dose-dependent cell death as the dose of radiation was increased. Additionally, the rate of apoptosis in the C17.2 NSCs reached 31.2 ± 1.23% in the 6 Gy irradiation group, which was the most significant when compared to the other irradiation treated groups. bFGF showed protective effect on cell apoptosis in a dose-dependent manner. The mean percentage of apoptotic cells decreased to 7.83 ± 1.75% when 100 ng/mL bFGF was given. Furthermore, U0126 could block the protective effect of bFGF by inhibiting the phosphorylation of ERK1/2.
conclusionsAn in vitro cellular model of radiation-induced apoptosis of NSCs, in C17.2 NSCs, was developed successfully. Additionally, bFGF can protect neurons from radiation injury in vitro via the ERK1/2 signal transduction pathway.
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