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International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

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Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

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Article

NF-κB signaling modulates radiation‑induced microglial activation

  • Authors:
    • Jun Xue
    • Ji-Hua Dong
    • Guo-Dong Huang
    • Xiao-Fei Qu
    • Gang Wu
    • Xiao-Rong Dong
  • View Affiliations / Copyright

    Affiliations: Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
  • Pages: 2555-2560
    |
    Published online on: April 23, 2014
       https://doi.org/10.3892/or.2014.3144
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Abstract

Microglial activation has been suggested to be associated with the incidence of radiation-induced brain injury. The present study investigated the molecular mechanism(s) involved in radiation-induced activation of the microglia. Mouse microglial BV-2 cells were exposed to different doses of radiation. The release of inflammatory factors was evaluated by enzyme-linked immunosorbent assay and real-time reverse transcriptase polymerase chain reaction. Protein expression was determined by immunocytochemistry and immunoblotting. Microglial activation was induced by radiation [>16 Gray (Gy)]. Activated cells exhibited a stouter spherical morphology and the levels of ionized calcium-binding adapter molecule-1 and CD68 were considerably upregulated. The generation of inflammatory factors, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6, toll‑like receptor 8 (TLR-8) and cyclooxygenase 2 (COX-2), was increased and peaked at either 3 or 6 h after radiation treatment. Phosphorylated γ-histone 2A, member X (γ-H2AX), which facilitates DNA double-strand breaks (DSBs), was upregulated at 3 h post-radiation treatment. This was accompanied by the nuclear translocation of the nuclear factor-κB (NF-κB) p65 subunit. Moreover, 3 h following radiation treatment, the NF-κB essential modulator (NEMO) was markedly elevated, whereas the NF-κB regulatory inhibitor-α (IκB-α) was considerably decreased. Our results demonstrate that the NF-κB signaling pathway may trigger microglial activation and release of inflammatory factors following irradiation. These findings may provide valuable insight into understanding the molecular mechanism(s) involved in brain injury induced by radiation therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Xue J, Dong J, Huang G, Qu X, Wu G and Dong X: NF-κB signaling modulates radiation‑induced microglial activation. Oncol Rep 31: 2555-2560, 2014.
APA
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., & Dong, X. (2014). NF-κB signaling modulates radiation‑induced microglial activation. Oncology Reports, 31, 2555-2560. https://doi.org/10.3892/or.2014.3144
MLA
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., Dong, X."NF-κB signaling modulates radiation‑induced microglial activation". Oncology Reports 31.6 (2014): 2555-2560.
Chicago
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., Dong, X."NF-κB signaling modulates radiation‑induced microglial activation". Oncology Reports 31, no. 6 (2014): 2555-2560. https://doi.org/10.3892/or.2014.3144
Copy and paste a formatted citation
x
Spandidos Publications style
Xue J, Dong J, Huang G, Qu X, Wu G and Dong X: NF-κB signaling modulates radiation‑induced microglial activation. Oncol Rep 31: 2555-2560, 2014.
APA
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., & Dong, X. (2014). NF-κB signaling modulates radiation‑induced microglial activation. Oncology Reports, 31, 2555-2560. https://doi.org/10.3892/or.2014.3144
MLA
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., Dong, X."NF-κB signaling modulates radiation‑induced microglial activation". Oncology Reports 31.6 (2014): 2555-2560.
Chicago
Xue, J., Dong, J., Huang, G., Qu, X., Wu, G., Dong, X."NF-κB signaling modulates radiation‑induced microglial activation". Oncology Reports 31, no. 6 (2014): 2555-2560. https://doi.org/10.3892/or.2014.3144
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