MicroRNA expression in vulvar lichen sclerosus keratinocytes and fibroblasts: further evidence and possible pathogenetic implications from an observational study.

Authors

Alessandro Borghi, Fernanda Martini, Lucilla D'Abundo, Cristian Bassi, Lucia Oton Gonzalez, Lucrezia Pacetti, Massimo Negrini, Monica Corazza

Published in

Italian journal of dermatology and venereology. Oct 08, 2026. Epub Oct 08, 2026.

Abstract

It seems established that genetic and epigenetic determinants drive the multifactorial pathogenic processes in vulvar lichen sclerosus (VLS). Aberrant expression of microRNAs (miRNAs) has been observed in a few studies suggesting their potential involvement. Our aim was to assess the expression of miRNAs both in VLS and in healthy keratinocytes and fibroblasts cultured separately.
In this observational study, five VLS and five healthy skin tissue specimens were used to derive independent keratinocyte and fibroblast cultures. Total RNA, including miRNA, was isolated from cells, quantified and used to prepare a miRNA library. The quality and quantity of miRNA libraries were analyzed and sequenced. Differentially expressed miRNAs have been identified using DESeq2 bioconductor package.
The differential analysis led to the identification of 171 and 111 microRNAs with an expression difference of at least 1.5-fold between VLS and healthy samples, in keratinocytes and fibroblasts, respectively. More than 80% of the 111 microRNAs identified as differentially expressed in fibroblasts were also found to be differentially expressed in keratinocytes. Several dysregulated miRNAs are involved in inflammation and fibrotic processes, namely miR-10a-5p and 3p, miR-143-3p and 5p, miR-181a-5p and 3p, miR-181b-5p and 3p, miR-21-3p, miR-146b-5p and miR-29c.
Our results showed a clear separation of VLS keratinocytes and fibroblasts from healthy cells in terms of miRNA expression. It is noteworthy that the most dysregulated miRNAs are implicated in inflammatory and fibrotic pathways. It is conceivable that miRNA expression is functional in regulating pathogenetic mechanisms of LS.

PMID:
42844977
Bibliographic data and abstract were imported from PubMed on 08 Oct 2026.

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