Background: Light at visible spectrum has been associated with anti-inflammatory and anti-aging effects. Ultraviolet A (UVA) radiation is the most important environmental factor associated with exogenous aging via induction of reactive oxygen species (ROS). Objective: In this study, we focused on elucidating the molecular mechanisms involved in biological effects associated with 590. nm light delivered from light emitting diode (LED). Methods: UVA-induced metalloproteinase-1 (MMP-1) expression in dermal fibroblast was used as a model system for investigation. Results: Pretreating cultured human fibroblasts with 590. nm light attenuated UVA-induced ROS, phosphorylated Jun N-terminal kinases, and MMP-1 expressions in a sequential manner. Pretreatment with potent antioxidant N-acetylcysteine produced similar effect, suggesting enhanced antioxidant capacity induced by 590. nm photomodulation. Further experiments demonstrated that 590. nm photomodulation attenuated UVA-induced ROS and MMP-1 expressions via mitochondrial retrograde signaling that augments the antioxidant enzyme expression in a peroxisome proliferators-activated receptor γ coactivator-1α-dependent manner. Conclusion: Our results provided possible mechanistic insights explaining the effect of visible light on treating clinical conditions associated with ROS-mediated dysfunctions.
Date:
2015-05
Relation:
Journal of Dermatological Science. 2015 May;78(2):125-132.
