ArticleCell death & disease2023
WFDC12-overexpressing contributes to the development of atopic dermatitis via accelerating ALOX12/15 metabolism and PAF accumulation.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- Imaging transcriptomics in basal cell carcinoma: Coupling in vivo tumor morphology with gene expression.JID innovations : skin science from molecules to population health · 2026Article
- Genetic Liability to COPD and Periodontitis Risk: Integrative Genetic and Single-Cell Evidence Implicating Macrophage Reprogramming.International journal of chronic obstructive pulmonary disease · 2026Article
- Ameliorative effects of squid phospholipids from Todarodes pacificus on atopic dermatitis-like lesions in NC/Nga mice.Archives of dermatological research · 2025Article
- Genetic effects on the skin methylome in healthy older twins.American journal of human genetics · 2024Article
- Selenomethionine in gelatin methacryloyl hydrogels: Modulating ferroptosis to attenuate skin aging.Bioactive materials · 2024Article
- IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells.International journal of biological sciences · 2024Article
- Versatile whey acidic protein four-disulfide core domain proteins: biology and role in diseases.Frontiers in cell and developmental biology · 2024Review
- Construction of a novel pyrotosis-related prognostic model of esophageal square cell carcinoma and determination of the anti-tumor effect of WFDC12.Functional & integrative genomics · 2023Article
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Authors and funding
17 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by eczema-like skin lesions, dry skin, severe itching, and recurrent recurrence. The whey acidic protein four-disulfide core domain gene WFDC12 is highly expressed in skin tissue and up-regulated in the skin lesions of AD patients, but its role and relevant mechanism in AD pathogenesis have not been studied yet. In this study, we found that the expression of WFDC12 was closely related to clinical symptoms of AD and the severity of AD-like lesions induced by DNFB in transgenic mice. WFDC12-overexpressing in the epidermis might promote the migration of skin-presenting cells to lymph nodes and increase Th cell infiltration. Meanwhile, the number and ratio of immune cells and mRNA levels of cytokines were significantly upregulated in transgenic mice. In addition, we found that ALOX12/15 gene expression was upregulated in the arachidonic acid metabolism pathway, and the corresponding metabolite accumulation was increased. The activity of epidermal serine hydrolase decreased and the accumulation of platelet-activating factor (PAF) increased in the epidermis of transgenic mice. Collectively, our data demonstrate that WFDC12 may contribute to the exacerbation of AD-like symptoms in DNFB-induced mouse model by enhancing arachidonic acid metabolism and PAF accumulation and that WFDC12 may be a potential therapeutic target for human atopic dermatitis.
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