Polydeoxyribonucleotide promotes cyclobutane pyrimidine dimer repair in UVB-exposed dermal fibroblasts
Open accessAbstract
Background: DNA is the main cellular chromophore for ultraviolet B (UVB). Its absorption leads to the generation of typical photoproducts. The most frequent types (about 80%) are cyclobutane pyrimidine dimers (CPDs). Several studies have suggested that treatment with deoxyribonucleosides can protect some cell types from DNA damage. The aim of this work was to evaluate the ability of the polydeoxyribonucleotide (PDRN) to protect human dermal fibroblasts from UVB‐induced DNA damage. Methods: Human dermal fibroblasts were irradiated with 600 mJ/cm 2 of UVB radiation. Cells were analyzed at increasing time points from irradiation to study the recovery from UVB‐induced DNA photodamage. Damage repair was subsequently assessed by immunocytochemical analysis of CPDs levels and by measurement of p53 protein expression. Results: The extracellular addition of 100 μg/ml PDRN immediately after irradiation caused a strong activation of p53 protein in the first 24 h. This signal was accompanied by an increase in CPDs repair rates at early time points of recovery. Conclusions: The addition of PDRN to the culture medium supports CPDs repair probably providing a faster supply of precursors for the deoxyribonucleotide triphosphates pool necessary to UVB‐damaged cells. This condition could promote the action of the salvage pathway, thereby accelerating DNA repair, but other inducible responses linked to increased p53 expression could be involved.
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In dermal fibroblasts, PDRN enhances metabolic activity and promotes the synthesis of collagen types I and III through activation of the ERK pathway.
“In dermal fibroblasts, PDRN enhances metabolic activity and promotes the synthesis of essential ECM components—particularly collagen types I and III—through activation of the extracellular signal-regulated kinase (ERK) pathway [52,89,90,91,92,93,94].”
From Comparison of Polynucleotide and Polydeoxyribonucleotide in Dermatology: Molecular Mechanisms and Clinical Perspectives (2025) · cites this paper as [90]
The Results (p53 levels; page unavailable) and Discussion (page unavailable) report that PDRN increased p53 expression and accelerated repair of UVB-induced DNA damage in dermal fibroblasts. Searches for metabolic activity, collagen types I and III, and ERK found no passage addressing those claimed effects or mechanism. (LLM, conf=0.76)
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- Authors
- Belletti, S., Uggeri, J., Gatti, R., Govoni, P., & Guizzardi, S.
- Affiliations
- University of Parma (IT)
- Corresponding author
- Guizzardi, Stefano
- Venue
- Photodermatology, Photoimmunology & Photomedicine
- Publisher
- Wiley
- Published
- 2007-11
- Volume
- 23
- Issue
- 6
- Pages
- 242-249
- ISSN
- 0905-4383 (ISSN-L)
- 1600-0781
- OpenAlex
- W2083633975
- Cited by
- 38
- References
- 3
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 8 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 3 · 2014: 1 · 2013: 2
- FWCI
- 0.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Photodermatology Photoimmunology & Photomedicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Università degli Studi di Parma (FIL 2005)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- polydeoxyribonucleotide, cyclobutane pyrimidine dimers, UVB-induced DNA damage, DNA repair, dermal fibroblasts, p53 expression, salvage pathway, deoxyribonucleosides, photoproducts, UVB protection
- MeSH terms
- Cells, Cultured, DNA, DNA Repair, Fibroblasts, Humans, Polydeoxyribonucleotides, Pyrimidine Dimers, Ultraviolet Rays, Tumor Suppressor Protein p53
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