Ultraviolet B (UVB) in sunlight cause skin damage ranging from wrinkles to photoaging and skin cancer. UVB can affect genomic DNA by creating cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidine (6-4) photoproducts (6-4PPs). These lesions are mainly repaired by nucleotide excision repair (NER) system and by photolyase enzymes that are activated by blue light. Our main goal was to validate the use of "Xenopus laevis" as an in vivo model system for investigating the impact of UVB on skin physiology. The mRNA expression levels of xpc and six other genes of the NER system and CPD/6-4PP photolyases were found at all stages of embryonic development and in all adult tissues tested. When examining Xenopus embryos at different time points after UVB irradiation, we observed a gradual decrease in CPD levels, an increased number of apoptotic cells together with an epidermal thickening and an increased dendricity of melanocytes. We observed a quick removal of CPDs when embryos are exposed to blue-light versus in the dark confirming the efficient activation of photolyases. A decrease in the number of apoptotic cells and an accelerated return to normal proliferation rate was noted in blue-light exposed embryos compared to their control counterparts. Overall, gradual decrease in CPD levels, detection of apoptotic cells, and thickening of epidermis and increased dendricity of melanocytes recapitulate human skin responses to UVB and support Xenopus as an appropriate and alternative model for such studies. This article is protected by copyright. All rights reserved.
Keyphrases
- induced apoptosis
- cell death
- cell cycle arrest
- cell free
- signaling pathway
- soft tissue
- wound healing
- gene expression
- oxidative stress
- endoplasmic reticulum stress
- anti inflammatory
- radiation therapy
- genome wide
- dna methylation
- young adults
- cell proliferation
- radiation induced
- light emitting
- transcription factor
- single molecule
- quantum dots