These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: PINK1 in normal human melanocytes: first identification and its effects on H2 O2 -induced oxidative damage.
    Author: Wang L, Ding X, Huang H, Li Z, Li M, Du J, Zhang J.
    Journal: Clin Exp Dermatol; 2021 Mar; 46(2):292-299. PubMed ID: 32870534.
    Abstract:
    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: Quantitative reverse transcription-PCR and western blot analysis were used to analyse the expression of PINK1 in PIG1 melanocyte and gene downregulation models. Levels of cell viability, cell apoptosis and intracellular reactive oxygen species (ROS), mitochondrial morphology, mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (MPTP) opening were measured in PIG1 models transfected with PINK1 small interfering RNA with or without hydrogen peroxide (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 in mitochondria, decreased the MMP and increased MPTP opening. CONCLUSIONS: Our study found PINK1 plays an essential role in protecting human melanocytes from oxidative stress.
    [Abstract] [Full Text] [Related] [New Search]