Activation of transient receptor potential vanilloid 3 is required for keratinocyte differentiation and epidermal barrier formation
Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca² signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3...
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| Published in | The Korean journal of physiology & pharmacology Vol. 29; no. 4; pp. 409 - 418 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
The Korean Physiological Society and The Korean Society of Pharmacology
01.07.2025
대한약리학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1226-4512 2093-3827 2093-3827 |
| DOI | 10.4196/kjpp.24.324 |
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| Abstract | Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²
signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca
]
changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders. |
|---|---|
| AbstractList | Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca2+]i changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders. Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca2+]i changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders. KCI Citation Count: 0 Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca² signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca ] changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders. Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca2+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca2+]i changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders.Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca2+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and triggers the release of pro-inflammatory cytokines, causing inflammation and itching. However, the regulation of skin barrier recovery by TRPV3 and its expression during keratinocyte differentiation remain unexplored. This study aimed to investigate the role and expression levels of TRPV3 in keratinocyte differentiation and skin barrier recovery, focusing on the effects of varying TRPV3 activation using pharmacological agents. Differentiation of primary human keratinocytes was induced in high-calcium media, and TRPV3 activity and expression were assessed using patch-clamp, fura-2 fluorimetry, and immunoblotting. The effects of TRPV3 agonists on skin barrier recovery following tape stripping were evaluated by measuring transepidermal water loss in mice. Results showed that TRPV3 expression, current density, and agonist-induced [Ca2+]i changes increased with keratinocyte differentiation. The TRPV3 antagonist, ruthenium red, inhibited both keratinocyte differentiation and TRPV3 upregulation. TRPV3 agonists (2-APB/carvacrol) facilitated early differentiation but paradoxically downregulated TRPV3 expression at higher concentrations. Moderate TRPV3 activation by lower agonist concentrations enhanced skin barrier recovery, while higher concentrations hindered recovery and induced immune cell infiltration. These findings highlight the dual role of TRPV3 in skin homeostasis and suggest that targeted modulation of TRPV3 could be a promising strategy for treating skin disorders. |
| Author | Kim, Woo Kyung Jeon, Young Keul Chung, Elina Da Sol Kim, Hyun Jong Nam, Yu Ran Park, Kyung Sun Nam, Joo Hyun Kim, Sung Joon |
| AuthorAffiliation | 4 Wide River Institute of Immunology, Seoul National University College of Medicine, Hongcheon 25159, Korea 3 Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea 5 Department of Internal Medicine, Dongguk University Graduate School of Medicine, Goyang 10326, Korea 2 Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea 1 Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea |
| AuthorAffiliation_xml | – name: 3 Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea – name: 4 Wide River Institute of Immunology, Seoul National University College of Medicine, Hongcheon 25159, Korea – name: 5 Department of Internal Medicine, Dongguk University Graduate School of Medicine, Goyang 10326, Korea – name: 1 Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea – name: 2 Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea |
| Author_xml | – sequence: 1 givenname: Elina Da Sol surname: Chung fullname: Chung, Elina Da Sol organization: Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea – sequence: 2 givenname: Yu Ran surname: Nam fullname: Nam, Yu Ran organization: Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea – sequence: 3 givenname: Hyun Jong surname: Kim fullname: Kim, Hyun Jong organization: Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea, Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea – sequence: 4 givenname: Young Keul surname: Jeon fullname: Jeon, Young Keul organization: Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea – sequence: 5 givenname: Kyung Sun surname: Park fullname: Park, Kyung Sun organization: Wide River Institute of Immunology, Seoul National University College of Medicine, Hongcheon 25159, Korea – sequence: 6 givenname: Woo Kyung surname: Kim fullname: Kim, Woo Kyung organization: Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea, Department of Internal Medicine, Dongguk University Graduate School of Medicine, Goyang 10326, Korea – sequence: 7 givenname: Sung Joon surname: Kim fullname: Kim, Sung Joon organization: Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea, Wide River Institute of Immunology, Seoul National University College of Medicine, Hongcheon 25159, Korea – sequence: 8 givenname: Joo Hyun surname: Nam fullname: Nam, Joo Hyun organization: Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea, Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40288993$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART003219535$$DAccess content in National Research Foundation of Korea (NRF) |
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| Keywords | Keratinocytes TRPV cation channels Inflammation Cell differentiation Skin physiology |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Author contributions: E.D.S.C. performed formal analysis, investigation, visualization and wrote the original draft. Y.R.N., H.J.K., and Y.K.J. performed formal analysis, investigation, and visualization. K.S.P. conducted formal analysis, investigation, and provided resources. W.K.K. conceptualized the study, supervised, managed project administration, and reviewed and edited the manuscript. S.J.K. conceptualized the study, reviewed and edited the manuscript, and managed project administration. J.H.N. conceptualized the study, wrote the original draft, supervised, managed project administration, and reviewed and edited the manuscript. |
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| Snippet | Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²
signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and... Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca2+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and... Transient receptor potential vanilloid 3 (TRPV3)-mediated Ca²+ signaling in keratinocytes plays a crucial role in epidermal keratinocyte differentiation and... |
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| Title | Activation of transient receptor potential vanilloid 3 is required for keratinocyte differentiation and epidermal barrier formation |
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