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Molecular Evidence on Activation of pro‐inflammatory NF‐κB Signaling Pathway by X‐ray Irradiation
Author(s) -
Chung Hae Young,
Chung Sang Woon,
Kim Ji Young,
Go Eun Kyung,
Kim Ji Min,
Choi Jae Hun,
Lim Hyun Ae,
Lim Hyeong Kwan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.298
Subject(s) - signal transduction , nf κb , oxidative stress , transcription factor , mapk/erk pathway , microbiology and biotechnology , chemistry , reactive oxygen species , phosphorylation , redox , inflammation , p38 mitogen activated protein kinases , proinflammatory cytokine , biology , gene , biochemistry , immunology , organic chemistry
The biological effects of x‐ray irradiation are a cause of oxidative damage and cellular redox imbalance. In the present study, we investigated the molecular mechanisms underlying irradiation‐induced alteration of signal pathways by closely examining a redox‐sensitive transcription factor, NF‐κB and various pro‐inflammatory gene expressions. Our results clearly showed that a short‐term irradiation can readily alter signal pathways causing NF‐κB activation. Furthermore, we obtained molecular evidence showing the up‐regulation of major NF‐κB‐dependent pro‐inflammatory genes such as COX‐2, iNOS, VCAM1, ICAM1, and E‐selectin. We also found that X‐ray irradiation caused oxidative stress to these animals which led to a dose‐dependent redox imbalance as shown by key redox markers. Our findings on phosphorylated ERK, JNK, and p38 MAPKs further revealed molecular insights into the pro‐inflammatory activation of X‐ray irradiation. The significance of the current study is the new molecular information on the up‐regulation of various pro‐inflammatory genes through NF‐κB activation via the MAPKs pathway. We propose that the major biological damaging effect of X‐ray irradiation may be the subtle activation of inflammatory processes through the disruption of redox‐sensitive cellular signaling pathways. [This work was supported by KOSEF grant funded by the Korea government (MOST) (NO. 2007‐00376).]