Expression of the autophagic markers, light chain 3-I, light chain 3-II, and beclin 1, in vitiligo: a case-control study

• Published in: Journal of the Egyptian Women’s Dermatologic Society Vol. 18; no. 2; pp. 89 - 96
• Main Authors: El-Hanafy, Ghada, Nada, Hanan, Rashed, Laila, Mousa, Marwa, Elmasry, Maha
• Format: Journal Article
• Language: English
• Published: Wolters Kluwer India Pvt. Ltd 01.05.2021; Medknow Publications and Media Pvt. Ltd; Wolters Kluwer Medknow Publications
• Subjects: Analysis; autophagy; beclin 1; light chain 3-i; light chain 3-ii; Medical research; Medicine, Experimental; oxidative stress; Superoxide; vitiligo; vitiligo; beclin 1; autophagy; light chain 3-II; light chain 3-I; oxidative stress
• ISSN: 1687-1537; 2090-2565; 2090-2565
• DOI: 10.4103/jewd.jewd_53_20

Background Autophagy is a lysosomal degradative process that is essential for the cell viability, homeostasis, and maintenance. Objective To measure microtubule-associated protein 1 light chain 3 (LC3)-I, LC3-II, and beclin 1 as indicators of autophagy and superoxide dismutase (SOD) and malondialdehyde (MDA) as indicators of oxidative stress in patients with vitiligo. Patients and methods This comparative case-control study was conducted on 20 patients with nonsegmental vitiligo as well as 20 controls. LC3-I, LC3-II, and beclin 1 tissue expressions were detected by western blot analysis, whereas MDA and SOD were measured by the colorimetry method in the tissue homogenate. Results The LC3-I, LC3-II, beclin 1, and SOD levels were significantly lower in lesional skin than nonlesional skin of patients as well as both lesional and nonlesional skin of patients than controls (P<0.001). On the contrary, the level of MDA was significantly higher in lesional skin than nonlesional skin of patients as well as both lesional and nonlesional skin of patients than controls (P<0.001). Conclusion Downregulated autophagy as evident by downregulated levels of autophagic markers together with dysregulated oxidative stress species could play a role in the pathogenesis of vitiligo, and optimizing autophagy could open a new era in vitiligo treatment.