To Control Site-Specific Skin Gene Expression, Autocrine Mimics Paracrine Canonical Wnt Signaling and Is Activated Ectopically in Skin Disease

    Dong-Won Kim, M. Zulfiquer Hossain, Ashley Nieves, Lihong Gu, Tabetha S. Ratliff, Seung Mi Oh, Angela Park, Sang Seop Han, Nicole B. Yang, Ji Qi, Janis M. Taube, Sewon Kang, Luis A. Garza
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    TLDR The research suggests that a specific skin gene can be controlled by signals within and between cells and is wrongly activated in certain skin diseases.
    The document details a study on the regulation of KRT9, a gene associated with the thick, hairless skin of the palms and soles (volar skin). The research found that KRT9 can be expressed in keratinocytes both independently and when co-cultured with volar fibroblasts, with higher expression levels in the presence of fibroblasts. The study demonstrated that canonical Wnt/β-catenin signaling is crucial for KRT9 expression, which can be activated through both autocrine and paracrine mechanisms. Additionally, the study observed ectopic expression of KRT9 in skin diseases like lichen simplex chronicus, suggesting a disruption of site-specific gene expression. The findings propose a new understanding of skin gene expression regulation and potential therapeutic applications for skin identity reprogramming. The number of human subjects or samples used in the study was not provided, except for a mention of three subjects in one cohort, limiting the ability to assess the study's strength based on sample size.
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