Hsa-miR-31-3p targets CLDN8 to compromise skin barrier integrity in psoriasis.

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 exper

SUBMITTER: Tu Y 

PROVIDER: S-EPMC11954119 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature