ArticleCell death & disease2022
Activation of the JNKs/ATM-p53 axis is indispensable for the cytoprotection of dermal fibroblasts exposed to UVB radiation.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- A TERRA-NONO axis drives fibroblast reprogramming in cancer.Science advances · 2026Article
- Isoflavone-Rich Fraction of Traditional Thai Fermented Soybean (Thua Nao) Protects Dermal Fibroblasts from Photoaging by Modulating MAPK and Akt Signaling Pathways.International journal of molecular sciences · 2026Article
- Time- and dose-dependent regulation of circular RNAs in the response of triple-negative breast cancer cells to ionizing radiation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Phenoxazine Derivative ST61 Displays an Oxidative-Stress-Mediated Cytotoxic Activity Against Human Cancer Cells.Biomolecules · 2026Article
- Identification of Hub genes in melasma using integrated transcriptomic analysis.Bioinformation · 2026Article
- Establishing an Improved Cellular Photoaging Model by Repeated UVA Exposure of Human Skin Fibroblasts.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2025Article
- Methyl jasmonate elicitation enhances photoprotective and anti-inflammatory properties in Lavandula angustifolia cell suspension cultures.Scientific reports · 2025Article
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- Accumulation Kinetics and Biological Action of Doxorubicin in Rabbit Intervertebral Discs.International journal of molecular sciences · 2025Article
- Screening of a Plant Extract Library from the Greek Flora for Biological Activities Related to Anti-Aging Applications.Antioxidants (Basel, Switzerland) · 2025Article
- Biochemical Mechanism of Thai Fermented Soybean Extract on UVB-Induced Skin Keratinocyte Damage and Inflammation.International journal of molecular sciences · 2025Article
- A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence.Aging cell · 2025Article
- Recent advances in dermal fibroblast senescence and skin aging: unraveling mechanisms and pioneering therapeutic strategies.Frontiers in pharmacology · 2025Review
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- Effects of Akt Activator SC79 on Human M0 Macrophage Phagocytosis and Cytokine Production.Cells · 2024Article
- CLCA2: A Potential Guardian against Premature Senescence and Skin Aging.Biomedicines · 2024Article
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- Biological Activities ofInternational journal of molecular sciences · 2023Article
- The Effect of Carnosine on UVA-Induced Changes in Intracellular Signaling of Human Skin Fibroblast Spheroids.Antioxidants (Basel, Switzerland) · 2023Article
- Anthocyanin fromClinical, cosmetic and investigational dermatology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Although UVB radiation is mainly absorbed by the epidermis, ~5-10% of its photons reach and affect the upper part of the dermis. Physiologically relevant UVB doses, able to provoke erythema, induce apoptosis in human dermal fibroblasts in vitro, as well as in the dermis of SKH-1 mice. Given the sparse and even contradictory existing information on the effect of UVB radiation on dermal fibroblasts' viability, aim of this work was to unravel the crucial signaling pathways regulating the survival of UVB-treated human dermal fibroblasts. We found that UVB radiation immediately stimulates the phosphorylation of MAPK family members, as well as Akt, and is genotoxic leading to the delayed ATM-p53 axis activation. Akt phosphorylation after UVB radiation is EGFR-mediated and EGFR inhibition leads to a further decrease of viability, while the Akt activator SC79 rescues fibroblasts to an extent by a mechanism involving Nrf2 activation. The known Nrf2 activator sulforaphane also exerts a partial protective effect, although by acting in a distinct mechanism from SC79. On the other hand, inhibition of JNKs or of the ATM-p53 axis leads to a complete loss of viability after UVB irradiation. Interestingly, JNKs activation is necessary for p53 phosphorylation, while the ATM-p53 pathway is required for the long-term activation of JNKs and Akt, reassuring the protection from UVB. Although UVB radiation results in intense and prolonged increase of intracellular ROS levels, classical anti-oxidants, such as Trolox, are unable to affect Akt, JNKs, or p53 phosphorylation and to reverse the loss of fibroblasts' viability. Collectively, here we provide evidence that the main viability-regulating UVB-triggered biochemical pathways act synergistically towards the protection of human dermal fibroblasts, with EGFR/Akt and Nrf2 serving as auxiliary anti-apoptotic machineries, while JNKs/ATM-p53 activation and interplay being overriding and indispensable for the perpetuation of cellular defense and the maintenance of cell viability.
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