820 Blue Light Exposure Rapidly Enhances HO-1 Production in Monocytic Cells

Friday, March 23, 2012: 2 p.m. - 3:15 p.m.
Presentation Type: Poster Session
Y. TOMLINSON, N. ECHOLS, V. MCCLOUD, P. LOCKWOOD, R. MESSER, and J. LEWIS, Georgia Health Sciences University, Augusta, GA
Objective: Previous studies have shown that blue light (400-500 nm) activates the redox-responsive Nrf2 signaling pathway. Heme oxygenase-1 (HO-1, regulated by Nrf2) is a cytoprotective protein that has been shown to limit the inflammatory response and is upregulated by blue light in a variety of epithelial and fibroblast cell types. We hypothesized that blue light exposure could enhance production of HO-1 mRNA and protein in immune cells as well. This research focused on the extent and time course of this response in THP-1 monocytic cells.

Method: THP-1 cells (n = 3) were treated with blue light (45 J/cm2) delivered from a quartz-tungsten-halogen dental curing light (VIP, Bisco, 600 mW/cm2). Controls received no light exposure. Proteins were extracted at 5, 10, 15, 30, and 60 min post-light treatment, then separated by SDS-PAGE, identified by Western blot analysis, and quantified (Odyssey®) to assess blue light-induced changes in levels of HO-1. Parallel experiments were performed to harvest RNA for quantitative RT-PCR analysis of HO-1 mRNA levels. Changes in HO-1 protein or mRNA levels were analyzed by ANOVA and Tukey post-hoc comparisons (α = 0.05).

Result: Western blot analysis revealed that blue light rapidly and significantly elevated HO-1 mRNA levels (p < 0.05) in THP-1 cells.  Likewise, HO-1 mRNA levels rapidly increased and peaked with a 2.6-fold increase at 10 min.  However, HO-1 mRNA levels remained elevated through the 60 min time point (1.9-fold).  

Conclusion: THP-1 monocytic cells respond to blue light exposure by rapidly and significantly increasing production of the cytoprotective HO-1 protein.  This response may be useful in limiting inflammation in the oral cavity.  

Keywords: Biochemistry, Cell culture, Curing lights, Inflammation and Inflammatory mediators