Blue Light Irradiation Induces Human Keratinocyte Cell Damage via Transient Receptor Potential Vanilloid 1 (TRPV1)
Ju Ah Yoo1, Eunbi Yu1, See-Hyoung Park2
1Molecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, 16419 Gyunggi Do, Republic of Korea.
Abstract:
Although blue light has been reported to affect skin cells negatively, little is known about its action mechanisms in skin cells. Therefore, we investigated the role of the transient receptor potential vanilloid 1 (TRPV1) in blue light-induced effects on human keratinocytes and its underlying mechanisms. Blue light decreased cell proliferation and upregulated TRPV1 expression. Blue light also suppressed the epidermal growth factor receptor- (EGFR-) mediated signaling pathway by reducing the protein levels of EGFR and suppressing the EGFR/PI3K/AKT/GSK3β/FoxO3a pathway. The blue light-induced effect in cell proliferation was reversed by TRPV1 siRNA, but not capsazepine, a TRPV1-specific antagonist. In addition, blue light irradiation increased the production of reactive oxygen species (ROS) and tumor necrosis factor-α (TNF-α). Blue light irradiation also increased both phosphorylation levels of TRPV1 and calcium influx. The blue light-induced increase in production of ROS and TNF-α was reversed by capsazepine. Furthermore, the blue light-induced increase in production of TNF-α was attenuated by SP600125 or PDTC. These findings show that blue light regulates cell survival and production of ROS and TNF-α; its effects are mediated via TRPV1. Specifically, the effects of blue light on cell proliferation are mediated by upregulating TRPV1, a negative regulator of EGFR-FoxO3a signaling. Blue light-induced production of ROS and TNF-α is also mediated through increased calcium influx via TRPV1 activation.
Insights
Blue light negatively impacts skin cells by upregulating TRPV1 (transient receptor potential vanilloid 1), hindering cell proliferation and increasing inflammation. These effects are mediated by TRPV1 activation and calcium influx.
Area of Science:
- Dermatology
- Cell Biology
- Biochemistry
Background:
- Blue light exposure is increasingly common, yet its precise effects on skin cells remain unclear.
- Understanding the molecular mechanisms behind blue light's impact on skin is crucial for developing protective strategies.
Purpose of the Study:
- To investigate the role of transient receptor potential vanilloid 1 (TRPV1) in blue light-induced effects on human keratinocytes.
- To elucidate the underlying mechanisms of blue light's action on skin cell proliferation, signaling pathways, and inflammatory responses.
Main Methods:
- Human keratinocytes were exposed to blue light.
- TRPV1 expression, cell proliferation, epidermal growth factor receptor (EGFR) signaling, reactive oxygen species (ROS), and tumor necrosis factor-alpha (TNF-α) production were analyzed.
- TRPV1 was modulated using siRNA and the antagonist capsazepine.
Main Results:
- Blue light decreased keratinocyte proliferation and upregulated TRPV1 expression.
- Blue light suppressed EGFR signaling and reduced key pathway proteins.
- Blue light increased ROS and TNF-α production, TRPV1 phosphorylation, and calcium influx.
- TRPV1 siRNA reversed proliferation effects, while capsazepine reversed ROS and TNF-α production.
Conclusions:
- Blue light negatively affects skin cell survival and promotes inflammation via TRPV1.
- TRPV1 acts as a mediator for blue light's impact on cell proliferation, ROS, and TNF-α production through calcium influx.
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