Ablation of DJ-1 enhances oxidative stress by disturbing the function of mitochondria in epidermal melanocytes

Abstract

Background: Oxidative stress is implicated in the pathogenesis of vitiligo. The function of DJ-1 in oxidative damage of melanocytes is still elusive. Aims: The aim of this study was to investigate the role of DJ-1 in oxidative damage of melanocytes. Material and Methods: The expression of DJ-1 in melanocytes was studied by reverse transcription-quantitative polymerase chain reaction and Western blot. Short-interfering RNAs (siRNA) were employed to downregulate DJ-1. The cells were pooled into three groups: mock group (cells with transfection reagent), negative control (NC) group (negative siRNA control), and siRNA group. After H2O2treatment for 24 h, the morphological changes, cell viability, apoptosis, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP), and mitochondrial respiration were measured in different groups. Results: DJ-1 was highly expressed in PIG1 melanocytes. DJ-1 knockdown rendered PIG1 melanocytes more susceptible to oxidative stress. Loss of DJ-1 led to apoptosis of PIG1 cells by impairing the function of mitochondria, including morphological abnormalities, ROS accumulation, depolarization of MMP, less adenosine-triphosphate (ATP) production, and less proton leak. Conclusions: DJ-1 plays a role in maintaining the antioxidative capacity in epidermal melanocytes.

Keywords

• dj-1
• melanocyte
• mitochondria
• oxidative stress