Modulation of lipopolysaccharide-induced NF-κB signaling pathway by 635 nm irradiation via heat shock protein 27 in human gingival fibroblast cells.
Heat shock protein-27 (HSP27) is a member of the small HSP family which has been linked to the nuclear factor-kappa B (NF-κB) signaling pathway regulating inflammatory responses. Clinical reports have suggested that low-level light therapy/laser irradiation (LLLT) could be an effective alternative treatment to relieve inflammation during bacterial infection associated with periodontal disease. However, it remains unclear how light irradiation can modulate the NF-κB signaling pathway. We examined whether or not 635 nm irradiation could lead to a modulation of the NF-kB signaling pathway in HSP27-silenced cells and analyzed the functional cross-talk between these factors in NF-κB activation. The results showed that 635 nm irradiation led to a decrease in the HSP27 phosphorylation, reactive oxygen species (ROS) generation, I-κB kinase (IKK)/inhibitor of κB (IκB)/NF-κB phosphorylation, NF-κB p65 translocation and a subsequent decrease in the COX-1/2 expression and prostaglandin (PGE(2) ) release in lipopolysaccharide(LPS)-induced human gingival fibroblast cells (hGFs). However, in HSP27-silenced hGFs, no obvious changes were observed in ROS generation, IKK/IκB/NF-κB phosphorylation, NF-κB p65 translocation, nor in COX-1/2 expression, or PGE(2) release. This could be a mechanism by which 635 nm irradiation modulates LPS-induced NF-κB signaling pathway via HSP27 in inflammation. Thus, HSP27 may play a role in regulating the anti-inflammatory response of LLLT.
Department of Oral Pathology, School of Dentistry, Dental Science Research Institute, Chonnam National University, Gwangju, Korea.
WonBong
W
Lim
JiSun
J
Kim
SangWoo
S
Kim
Sandeep
S
Karna
JaeWoong
J
Won
Sang Mi
SM
Jeon
Seo Yeon
SY
Kim
YooDuk
Y
Choi
HongRan
H
Choi
OkJoon
O
Kim
D000328:Adult; D051545:Cyclooxygenase 1 / Q000235:genetics / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D005786:Gene Expression Regulation; D005881:Gingiva / Q000166:cytology / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D055551:HSP27 Heat-Shock Proteins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D051550:I-kappa B Kinase / Q000235:genetics / Q000378:metabolism; D007834:Lasers; D008027:Light; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016328:NF-kappa B / Q000235:genetics* / Q000378:metabolism; D010766:Phosphorylation; D061251:Primary Cell Culture; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction
D055551:HSP27 Heat-Shock Proteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D051550:I-kappa B Kinase; D015232:Dinoprostone