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Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9303285/ https://www.ncbi.nlm.nih.gov/pubmed/35038353 http://dx.doi.org/10.1111/exd.14530 |
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author | Vasas, Nikolett Pénzes, Zsófia Kistamás, Kornél Nánási, Péter Pál Molnár, Szabolcs Szegedi, Andrea Szöllősi, Attila Gábor Bíró, Tamás |
author_facet | Vasas, Nikolett Pénzes, Zsófia Kistamás, Kornél Nánási, Péter Pál Molnár, Szabolcs Szegedi, Andrea Szöllősi, Attila Gábor Bíró, Tamás |
author_sort | Vasas, Nikolett |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9303285 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93032852022-07-22 Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients Vasas, Nikolett Pénzes, Zsófia Kistamás, Kornél Nánási, Péter Pál Molnár, Szabolcs Szegedi, Andrea Szöllősi, Attila Gábor Bíró, Tamás Exp Dermatol Concise Communication 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. John Wiley and Sons Inc. 2022-02-04 2022-05 /pmc/articles/PMC9303285/ /pubmed/35038353 http://dx.doi.org/10.1111/exd.14530 Text en © 2022 The Authors. Experimental Dermatology published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Concise Communication Vasas, Nikolett Pénzes, Zsófia Kistamás, Kornél Nánási, Péter Pál Molnár, Szabolcs Szegedi, Andrea Szöllősi, Attila Gábor Bíró, Tamás Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title | Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title_full | Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title_fullStr | Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title_full_unstemmed | Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title_short | Transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
title_sort | transient receptor potential vanilloid 3 expression is increased in non‐lesional skin of atopic dermatitis patients |
topic | Concise Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9303285/ https://www.ncbi.nlm.nih.gov/pubmed/35038353 http://dx.doi.org/10.1111/exd.14530 |
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