ArticleInternational journal of molecular sciences2022
Altered Distribution and Expression of Syndecan-1 and -4 as an Additional Hallmark in Psoriasis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Syndecan-1 as a Biomarker for Cardiovascular Risk in Patients with Behçet's Disease.Archives of rheumatology · 2025Article
- Spatial and Functional Roles of Syndecans in Skin Wound Healing.International journal of molecular sciences · 2025Review
- Role of fibroblasts in nonfibrotic autoimmune skin diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Lack of Syndecan-1 promotes the pathogenesis of experimental rheumatoid arthritis.Immunogenetics · 2024Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Syndecans act as independent co-receptors to exert biological activities and their altered function is associated with many pathophysiological conditions. Here, syndecan-1 and -4 were examined in lesional skin of patients with psoriasis. Immunohistochemical staining confirmed altered syndecan-1 distribution and revealed absence of syndecan-4 expression in the epidermis. Fibronectin (FN)-known to influence inflammation and keratinocyte hyperproliferation via α5β1 integrin in psoriasis-was also decreased. Syndecan-1 and -4 expression was analyzed in freshly isolated lesional psoriatic human keratinocytes (PHK) characterized based on their proliferation and differentiation properties. mRNA levels of syndecan-1 were similar between healthy and PHK, while syndecan-4 was significantly decreased. Cell growth and release of the pro-inflammatory Tumor Necrosis Factor-alpha (TNFα) were selectively and significantly induced in PHKs plated on FN. Results from co-culture of healthy keratinocytes and psoriatic fibroblasts led to the speculation that at least one factor released by fibroblasts down-regulate syndecan-1 expression in PHK plated on FN. To assay if biological treatments for psoriasis target keratinocyte proliferation, gelatin-based patches enriched with inteleukin (IL)-17α or TNFα blockers were prepared and tested using a full-thickness healthy epidermal model (Phenion
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