ArticleMedical molecular morphology2021
Increased integrity of cell-cell junctions accompanied by increased expression of claudin 4 in keratinocytes stimulated with vitamin D3.
Article in Medical molecular morphology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Remodeling mechanisms and intervention strategies of the oral mucosal immune barrier.Frontiers in immunology · 2026Review
- Vitamin D boosts HIV-1 resistance in female genital epithelial cells by enhancing antiviral cathelicidin expression.Frontiers in immunology · 2026Article
- The Fate of Epidermal Tight Junctions in theInternational journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
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Abstract
The stratified squamous epithelium has a multilayer structure formed by the differentiation of the keratinized epithelium, which covers the skin and oral mucosa. The epithelium plays a central role in regulating the interactions between the immune system and pathogens. The tight junction (TJ) barrier, which is composed of adhesion molecules called claudins (CLDN), is critical for the homeostasis of the skin and oral mucosa. Furthermore, the crucial roles of vitamin D3 (VD3) in the pathogeneses of skin and oral mucosal disease have been suggested. The aim of this in vitro study was to observe the correlations between the integrity of the keratinocyte population and the expression levels of CLDN1 and CLDN4 in gingival epithelial cells, stimulated with VD3. CLDN 1 and 4 expression levels were down and upregulated, respectively, in the cells stimulated with VD3. Additionally, transepithelial electrical resistance (TEER) levels were increased in the stimulated cells when compared to the controls. These findings indicate that CLDN 4 may play a more important role in the TJ barrier than CLDN 1. Hence, the therapeutic effect of VD3 in skin and oral diseases may be regulated by the increase in the expression of CLDN 4.
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