Transient receptor potential vanilloid-3 (TRPV3) channel induces dermal fibrosis via the TRPV3/TSLP/Smad2/3 pathways in dermal fibroblasts
Abstract
Background Excessive wound healing can lead to hypertrophic scars, which are not only a cosmetic issue but could also be itchy or painful. Previously, we reported that, in comparison with normal tissue, thymic stromal lymphopoietin (TSLP) expression was increased in skin burn scars when the activation of transient receptor potential vanilloid-3 (TRPV3) of keratinocytes was increased. However, the functional role of TRPV3 in dermal fibrosis remains unclear.Objective We aimed to determine whether TRPV3 affects the collagen production of human primary dermal fibroblasts (HPDFs) and to investigate the mechanism involved.Method Human primary dermal fibroblasts were cultured and transformed into myofibroblasts using TSLP and carvacrol. Expression levels of α-SMA, fibronectin, and COL1A1 were determined using qPCR, western blotting, and immunofluorescence staining. Ca 2+ influx was measured using a calcium-sensitive fluorescent dye, Fura3-AM. Nuclear factor of activated T-cells (NFAT) and phosphorylated-Smad2/3 were determined by western blotting. Silencing of TRPV3 with TRPV3-specific small interference RNA was evaluated using qPCR and western blotting.Results The expression levels of α-SMA, fibronectin, COL1A1, and TSLP were significantly increased in carvacrol-treated HPDFs. The expression levels of α-SMA, fibronectin, and COL1A1 were significantly increased by TSLP. The expression levels of TSLP and COL1A1 were significantly blocked by TRPV3 silencing in HPDFs. Regulation of Ca 2+ influx and the expression levels of NFAT and p-Smad2/3 were significantly increased in carvacrol-treated HPDFs. ECM productions induced via the TRPV3/TSLP/Smad2/3 pathways.Conclusions The activation of the TRPV3 channels regulates dermal fibrosis by reducing extracellular matrix production via the TRPV3/TSLP/Smad2/3 pathways in dermal fibroblasts.
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Activation of TRPV3 channels regulates dermal structure by reducing ECM production via TRPV3/TSLP/Smad2/3 pathways in dermal fibroblasts.
“The activation of the TRPV3 channels regulates the dermal structure by reducing ECM production via the TRPV3/Thymic stromal lymphopoietin/Smad2/3 pathways in dermal fibroblasts [92].”
From Boosting the Photoaged Skin: The Potential Role of Dietary Components (2021) · cites this paper as [92]
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- Authors
- Um, J.-Y., Kang, S. Y., Kim, H. J., Chung, B. Y., Park, C. W., & Kim, H. O.
- Affiliations
- Hallym University Kangnam Sacred Heart Hospital (KR)
- Corresponding author
- Um, Ji-young
- Kang, Seok Young
- Kim, Hyun Ji
- Chung, Bo Young
- Park, Chun Wook
- Kim, Hye One
- Venue
- Journal of Dermatological Science
- Publisher
- Elsevier BV
- Published
- 2020-02
- Volume
- 97
- Issue
- 2
- Pages
- 117-124
- ISSN
- 0923-1811 (ISSN-L)
- OpenAlex
- W3000263092
- Cited by
- 43
- References
- 32
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 8 · 2023: 6 · 2022: 6 · 2021: 9 · 2020: 5
- FWCI
- 4.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Dermatological Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea (NRF-2017R1A2B4006252)
- Ministry of Health & Welfare, Republic of Korea (HI17C0597)
- Hallym University Research Fund (HURF-2017-35)
- Topics
- Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- TRPV3, skin fibrosis, thymic stromal lymphopoietin, Smad2/3 signaling, dermal fibroblasts, collagen synthesis, extracellular matrix, myofibroblast differentiation, carvacrol, calcium influx, NFAT, hypertrophic scars, burn scars, alpha-smooth muscle actin, fibronectin
- MeSH terms
- Cymenes, Thymic Stromal Lymphopoietin, Cell Differentiation, Cells, Cultured, Collagen, Extracellular Matrix, Fibroblasts, Fibrosis, Humans, Signal Transduction, Cytokines, Dermis, TRPV Cation Channels, Smad2 Protein, Smad3 Protein, Primary Cell Culture
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