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The Effect of Carnosine on UVA-Induced Changes in Intracellular Signaling of Human Skin Fibroblast Spheroids
Gilda Aiello1,2, Francesca Rescigno3, Marisa Meloni3
1Department of Human Science and Quality of Life Promotion, Telematic University San Raffaele, 00166 Rome, Italy.
Abstract:
Dermis fibroblasts are very sensitive to penetrating UVA radiation and induce photo-damage. To protect skin cells against this environmental damage, there is an urgent need for effective compounds, specifically targeting UVA-induced mitochondrial injury. This study aimed to analyze the effect of carnosine on the proteome of UVA-irradiated human skin fibroblast, cultured in a three-dimensional (3D) biological system recapitulating dermal compartment as a test system to investigate the altered cellular pathways after 48 h and 7 days of culture with or without carnosine treatment. The obtained results indicate that UVA dysregulates Oxidative Phosphorylation, the Fibrosis Signaling Pathway, Glycolysis I and Nrf2-mediated Oxidative Stress Response. Carnosine exercises provide a protective function against the harmful effects of UVA radiation by activating the Nrf2 pathway with the upregulations of some ROS-detoxifying enzymes such as the glutathione S-transferase (GST) protein family. Additionally, carnosine regulates the activation of the Epithelial Adherens Junction and Wound Healing Signaling Pathway by mediating the activation of structural proteins such as vinculin and zyxin as well as fibronectin 1 and collagen type XVIII alpha 1 chain against UVA-induced changes.
Insights
Carnosine protects skin fibroblasts from UVA damage by activating the Nrf2 pathway and upregulating antioxidant enzymes. It also supports wound healing pathways, mitigating photo-aging effects.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Dermal fibroblasts are susceptible to UVA radiation, leading to photo-damage.
- There is a need for compounds that protect skin cells from UVA-induced mitochondrial injury.
Purpose of the Study:
- To investigate the protective effects of carnosine on UVA-irradiated human skin fibroblasts.
- To analyze proteomic changes in fibroblasts treated with carnosine after UVA exposure.
Main Methods:
- Human skin fibroblasts were cultured in a 3D system mimicking the dermal compartment.
- Cells were exposed to UVA radiation with or without carnosine treatment.
- Proteomic analysis was performed after 48 hours and 7 days.
Main Results:
- UVA radiation disrupted Oxidative Phosphorylation, Fibrosis Signaling, Glycolysis I, and Nrf2-mediated Oxidative Stress Response.
- Carnosine activated the Nrf2 pathway, upregulating ROS-detoxifying enzymes like glutathione S-transferase (GST).
- Carnosine modulated Epithelial Adherens Junction and Wound Healing pathways, affecting proteins like vinculin, zyxin, fibronectin 1, and collagen type XVIII alpha 1.
Conclusions:
- Carnosine offers protection against UVA-induced photo-damage in dermal fibroblasts.
- Carnosine's protective mechanism involves activating the Nrf2 pathway and supporting cellular repair mechanisms.
