ArticleExperimental dermatology2022
Transient receptor potential vanilloid 3 expression is increased in non-lesional skin of atopic dermatitis patients.
Article in Experimental dermatology, 2022. 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, 14 citations in OpenAlex.
- Activation of transient receptor potential vanilloid 3 is required for keratinocyte differentiation and epidermal barrier formation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- TRPV3 in skin thermosensation and temperature responses.The journal of physiological sciences : JPS · 2025Review
- Inhibition of Cutaneous TRPV3 Channels by Natural Caffeic Acid for the Alleviation of Skin Inflammation.Molecules (Basel, Switzerland) · 2024Article
- N,N-Dimethylglycine Sodium Salt Exerts Marked Anti-Inflammatory Effects in Various Dermatitis Models and Activates Human Epidermal Keratinocytes by Increasing Proliferation, Migration, and Growth Factor Release.International journal of molecular sciences · 2023Article
- Heat promotes melanogenesis by increasing the paracrine effects in keratinocytes via the TRPV3/CaiScience · 2023Article
- TRPV3: Structure, Diseases and Modulators.Molecules (Basel, Switzerland) · 2023Review
- TRPV3 and Itch: The Role of TRPV3 in Chronic Pruritus according to Clinical and Experimental Evidence.International journal of molecular sciences · 2022Review
- Transient receptor potential vanilloid 3 expression is increased in non-lesional skin of atopic dermatitis patients.Experimental dermatology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
TRPV3 (transient receptor potential vanilloid 3) is a pro-inflammatory ion channel mostly expressed by keratinocytes of the human skin. Previous studies have shown that the expression of TRPV3 is markedly upregulated in the lesional epidermis of atopic dermatitis (AD) patients suggesting a potential pathogenetic role of the ion channel in the disease. In the current study, we aimed at defining the molecular and functional expression of TRPV3 in non-lesional skin of AD patients as previous studies implicated that healthy-appearing skin in AD is markedly distinct from normal skin with respect to terminal differentiation and certain immune function abnormalities. By using multiple, complementary immunolabelling and RT-qPCR technologies on full-thickness and epidermal shave biopsy samples from AD patients (lesional, non-lesional) and healthy volunteers, we provide the first evidence that the expression of TRPV3 is markedly upregulated in non-lesional human AD epidermis, similar to lesional AD samples. Of further importance, by using the patch-clamp method on cultured healthy and non-lesional AD keratinocytes, we also show that this upregulation is functional as determined by the significantly augmented TRPV3-specific ion current (induced by agonists) on cultured non-lesional AD keratinocytes when compared to healthy ones.
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