About the Presenter
Mauro Picardo, MD
Director of the Clinical and Experimental Department and of Cutaneous Physiopathology and Metabolomic Center
San Gallicano Dermatological Institute
Dr. Picardo worked in the field of acne and sebogenesis for a long period with a specific interest in lipidomic analysis and its modifications in acne.
He was trained at the Rome University “La Sapienza”. His main topics of interest are skin biochemistry, free radicals mediated damage of the skin, mechanism of control of skin pigmentation, and pigmentary disorders. As chairperson of the Integrated Center of Metabolomic Research (CIRM) at the San Gallicano Institute, coordinate lipidomic studies on acne and related disorders (seborrheic dermatitis, rosacea) in sebum and blood samples. His group has defined several collaborations with national and international research groups. He has served on the Board and President of national (SIDEMAST) and International (EIS, ESDR, ESPCR, IFPCS) scientific societies. In collaboration with Alain Taieb chair of the Vitiligo European Task Force and the Pigmentary disorders group of the EADV. Professor Picardo was the organizer of several national and international conferences (like the successful Acne Rosacea and related disease held in Rome in Dec 2009) and he is a member of the Editorial Board of some dermatological and biochemical journals including Pigment Cell and melanoma Research and Experimental Dermatology. He is the author of more than 300 publications in peer-reviewed journals (H index 60) and of more than 30 chapters in different books.
Possible Source of the Intracellular Oxidative Stress in Vitiligo
Take Home Message
The pathogenesis of the loss of melanocytes in patients with vitiligo is complex and involves the concurrent actions of multiple mechanisms, including genetic, immune-mediated, intrinsic, oxidative, and environmental factors. Although melanocyte loss is ultimately driven by cytotoxic CD8+ cells, the distinctive role of each involved element and the priming causes responsible for triggering the sequence of events culminating in the autoimmune-mediated melanocyte disappearance are yet to be highlighted. Oxidative stress has been considered one of the pathogenetic mechanisms involved in melanocyte disappearance. We have previously demonstrated that melanocytes also fibroblast from pigmented skin of patients with vitiligo present an increased intracellular ROS level associated with a pre-senescent phenotype. More recently, we described in vitiligo keratinocytes a defect of the differentiation process. All the cell populations examined presented an alteration of glucose metabolism and mitochondrial morphology. To evaluate whether a metabolic alteration generated oxidative stress, we assessed the role of a PPARy activator, capable of improving glucose metabolism, in controlling the phenomenon. The PPARy activator improved glucose metabolism, decreased ROS generation, and modified the biological behavior in all the cell cultures tested. Our results indicate that a metabolic abnormality characterizes the skin cell of vitiligo patients, which could be the basis of the continuous intracellular oxidative stress and the increased sensitivity to external stress. Prospectively a “metabolic” approach to the disease could be evaluated
Mauro Picardo, Federica Papaccio, Barbara Bellei, Andrea D’Arino, Daniela Kovacs, Emanuela Bastonini, Stefania Briganti, and Monica Ottaviani
Consultant for PPM, Incyte, Pfizer, however none is relevant for the presentation.