Expression of Antioxidant Response and Autophagy Markers in Patients with Vitiligo:An Immunohistochemical Study
- Author:
Eun Ji HONG
1
;
Hee Jung YOON
;
Ryung KWON
;
Young Lip PARK
;
Sul Hee LEE
;
SangHoon LEE
Author Information
1. Department of Dermatology, Soonchunhyang University Bucheon Hospital, Soonchunhyang University College of Medicine, Bucheon, Korea
- Publication Type:Original Article
- From:Korean Journal of Dermatology
2023;61(2):79-85
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:Oxidative stress is generally accepted as one of the principal pathogenesis of vitiligo, and keratinocyte-melanocyte interactions are also thought to play critical roles. It is well-known that antioxidant response and autophagy protect cells against oxidative damage, but the details and the compensatory relationship between the two mechanisms in the keratinocytes of vitiligo lesions remain unclear.
Objective:To evaluate the antioxidant response and autophagy status of patients with vitiligo and to explore the interactions between these two mechanisms.
Methods:Ten patients with clinicopathologically proven vitiligo and 10 normal controls were enrolled in our Department of Dermatology, Soonchunhyang University Hospital, Bucheon, Korea. Tissue samples of vitiligo lesions in the patient group and normal skin in the control group were immunohistochemically stained for nuclear factor erythroid 2-related factor 2 (Nrf2), Beclin-1, microtubule-associated protein light chain 3 (LC3)-II, and p62. The immunopositivity of epidermal keratinocytes was evaluated.
Results:Keratinocytes in vitiligo lesions had a significantly lower expression of Nrf2 (p=0.002) than that in the cells of normal controls. The levels of autophagy markers did not differ significantly between the two groups, but decreases in the Beclin-1 and LC3-II levels, and an increase in the p62 level in the patient group may indicate a small decrease in autophagy of patients with vitiligo.
Conclusion:Decreased antioxidant response and reduced autophagy may trigger melanocyte apoptosis in vitiligo lesions.
