In:
Photochemistry and Photobiology, Wiley, Vol. 89, No. 1 ( 2013-01), p. 199-207
Abstract:
Heat shock protein‐27 ( HSP 27) 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 HSP 27‐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 HSP 27 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 HSP 27‐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 HSP 27 in inflammation. Thus, HSP 27 may play a role in regulating the anti‐inflammatory response of LLLT .
Type of Medium:
Online Resource
ISSN:
0031-8655
,
1751-1097
DOI:
10.1111/php.2012.89.issue-1
DOI:
10.1111/j.1751-1097.2012.01225.x
Language:
English
Publisher:
Wiley
Publication Date:
2013
detail.hit.zdb_id:
2048860-9
SSG:
12
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