LED 590 nm photomodulation reduces UVA-induced metalloproteinase-1 expression via upregulation of antioxidant enzyme catalase. Issue 2 (May 2015)

• Record Type: Journal Article
• Authors: Lan, Cheng-Che E.; Ho, Pei-Yun; Wu, Ching-Shuang; Yang, Rei-Cheng; Yu, Hsin-Su
• Is Part Of: Journal of dermatological science. Volume 78:Issue 2(2015:May)
• Page Start: 125
• Page End: 132
• Publication Date: 2015-05
• Subjects: 590 nm light -- UVA -- Peroxisome proliferators-activated receptor γ coactivator-1α -- Reactive oxygen species -- Catalase; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2015.02.018
• Languages: English
• ISSNs: 0923-1811

Abstract

Highlights: We examine the biologic effects of 590 nm photomodulation on dermal fibroblasts. 590 nm light enhanced catalase expression via increased PGC1a. 590 nm light reduced UVA-induced intracellular ROS formation via catalase. 590 nm light may be used clinically for treating ROS-mediated dysfunctions. Abstract: 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.