Hsa-miR-31-3p targets CLDN8 to compromise skin barrier integrity in psoriasis
Year: 2025
Type: article
Abstract: Skin barrier dysfunction in psoriasis has emerged as a significant concern, yet the underlying molecular mechanisms remain incompletely understood. This study investigates the role of hsa-miR-31-3p in regulating skin barrier function through its interaction with claudin-8 (CLDN8) in psoriasis. Through analysis of clinical samples and public datasets, we observed significantly impaired skin barrier function in psoriasis patients, characterized by increased transepidermal water loss and decreased stratum corneum hydration. Notably, CLDN8 expression was markedly downregulated in psoriatic lesions, while hsa-miR-31-3p levels were elevated. Bioinformatics analysis and molecular studies revealed that hsa-miR-31-3p directly targets the 3′UTR of CLDN8, leading to its downregulation. In vitro experiments demonstrated that both CLDN8 knockdown and hsa-miR-31-3p overexpression compromised the permeability barrier in keratinocytes. Furthermore, in an imiquimod-induced psoriasis mouse model, administration of mmu-miR-31-3p antagomir effectively ameliorated skin barrier damage, reduced inflammatory manifestations, and restored CLDN8 expression. These findings unveil a novel mechanism whereby hsa-miR-31-3p regulates skin barrier function through CLDN8 in psoriasis, suggesting potential therapeutic strategies targeting this pathway for psoriasis treatment. • Study reveals new psoriasis mechanism: hsa-miR-31-3p/CLDN8 axis linked to skin barrier dysfunction. • Psoriasis lesions show high hsa-miR-31-3p, causing CLDN8 downregulation, a key tight junction protein. • CLDN8 downregulation damages skin barrier, driving psoriasis development and progression. • Targeting hsa-miR-31-3p/CLDN8 pathway could lead to new treatments for psoriasis patients. • Research provides in vitro and in vivo evidence, supporting its potential for clinical translation.
Authors: Yunhua Tu, Li Wang, Lijun An, Li He
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,700
OpenAlex ID: W4408408269