PINK1 in normal human melanocyte: first identification and its effects on H 2 O 2 ‐induced oxidative damage

Background Oxidative stress plays an important role in initiating the destruction of melanocytes, which could be one possible mechanism of vitiligo. PINK1 is an outer membrane protein of mitochondria, which protects many cells from oxidative stress through regulating mitochondrial function. However, the role of PINK1 and its effects on oxidative damage in melanocytes have not been elucidated. Aim To investigate the expression and effects of PINK1 on oxidative stress in human melanocytes. Methods RT-qPCR and Western blot analysis were used to analyze the expression of PINK1 in PIG1 melanocyte and gene downregulation models. Levels of cell viability, cell apoptosis, intracellular ROS, morphology of mitochondria, mitochondrial membrane potential and transition pore opening were measured in PIG1 transfected with PINK1 siRNA with or without H2 O2 . Results We first observed the expression of PINK1 in human PIG1 melanocytes and found that downregulation of PINK1 made melanocytes more sensitive to oxidative stress induced by H2 O2 with more cell apoptosis and increased intracellular ROS. Meanwhile, downregulation of PINK1 caused morphological changes of mitochondria, decreased mitochondrial membrane potential and increased MPTP opening. Conclusions Our study found PINK1 plays an essential role in protecting human melanocytes from oxidative stress.