Open AccessBasic Fibroblast Growth Factor Protects C 17.2 Cells from Radiation‐Induced Injury through ERK 1/2
Author(s) -
Luan Ping,
Zhou HaiHong,
Zhang Bei,
Liu AnMing,
Yang LianHong,
Weng XueLing,
Tao EnXiang,
Liu Jun
Publication year - 2012
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/j.1755-5949.2012.00365.x
Subject(s) - mapk/erk pathway , basic fibroblast growth factor , fibroblast growth factor , fibroblast growth factor receptor , fibroblast , chemistry , radiation injury , microbiology and biotechnology , biology , growth factor , biochemistry , medicine , signal transduction , radiation therapy , receptor , in vitro
Summary Aims To establish a radiation‐induced neural injury model using C 17.2 neural stem cells ( NSC s) and to investigate whether basic fibroblast growth factor ( bFGF ) can protect the radiation‐induced injury of C 17.2 NSC s. Furthermore, we aim to identify the possible mechanisms involved in this model. Methods C 17.2 NSC s 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 , ERK 1/2, and p‐ ERK 1/2 proteins was detected with or without U 0126 was pretreated prior to C 17.2 NSC s receiving irradiation. Results C 17.2 NSC s showed a dose‐dependent cell death as the dose of radiation was increased. Additionally, the rate of apoptosis in the C 17.2 NSC s 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, U 0126 could block the protective effect of bFGF by inhibiting the phosphorylation of ERK 1/2. Conclusions An in vitro cellular model of radiation‐induced apoptosis of NSC s, in C 17.2 NSC s, was developed successfully. Additionally, bFGF can protect neurons from radiation injury in vitro via the ERK 1/2 signal transduction pathway.