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Vitiligo involves the gradual disappearance of melanocytes, causing skin depigmentation. Long noncoding RNAs (lncRNAs), a type of noncoding RNA, are important for regulating inflammation and immunity. Despite this significance, there needs to be more published research on how lncRNAs are expressed in vitiligo cases and their potential roles in the biology of this skin condition. This study aims to elucidate the molecular landscape of vitiligo by analyzing gene expression profiles of vitiligo skin and normal skin. Two datasets, RNA-seq and microarray, were thoroughly investigated to identify differentially expressed (DE) genes and lncRNAs associated with vitiligo development. Functional enrichment analysis revealed biological processes and pathways influenced by dysregulated genes, highlighting intricate processes such as melanin biosynthesis and melanogenesis, shedding light on the complex regulatory networks involved in pigmentation and immune responses. Protein-protein interaction analysis highlighted significantly downregulated hub genes, including TYRP1, MLANA, MC1R, SLC45A2, PAX3, TYR, DCT, OCA2, PMEL, and SOX10, revealing significant functional relationships among identified hub genes within the network. RNA-seq data analysis uncovered DE-lncRNAs, emphasizing the regulatory role of lncRNAs in vitiligo. Moreover, the correlation analysis between the expression of lncRNAs and key genes associated with melanogenesis (OCA2, TYRP1, and PMEL) unveiled novel upregulated lncRNAs such as CRTC3-AS1, LCMT1-AS1, LINC02178 contributing to vitiligo development. Additionally, lncRNA-gene networks constructed based on key melanocyte-related genes provided insights into the molecular relationships relevant to vitiligo. Overall, this study offers a comprehensive understanding of vitiligo pathogenesis, identifying potential therapeutic targets and laying the foundation for future research in this critical area.
Fayez et al. (Wed,) studied this question.