Review article
UV-Radiation, Apoptosis and Skin
Nives Pustišek
Mirna Šitum
Abstract
Apoptosis or programmed cell death is a key function in regulating skin development, homeostasis and tumorigenesis.
The epidermis is exposed to various external stimuli and one of the most important is UV radiation. The UVA and UVB
spectra differ in their biological effects and in their depth of penetration through the skin layers. UVB rays are absorbed directly
by DNA which results in its damage. UVA can also cause DNA damage but primarily by the generation of reactive oxygen
species. By eliminating photodamaged cells, apoptosis has an important function in the prevention of epidermal
carcinogenesis. UV-induced apoptosis is a complex event involving different pathways. These include: 1. activation of the
tumour suppressor gene p53; 2. triggering of cell death receptors directly by UV or by autocrine release of death ligands; 3.
mitochondrial damage and cytochrome C release. The extrinsic pathway through death receptors such as fibroblast-associated,
tumour necrosis factor receptor and TNF related apoptosis inducing ligand receptor activate caspase cascade. The intrinsic
or mitochondrial pathway of apoptosis is regulated by the Bcl-2 family of proteins, anti-apoptotic (Bcl-2, Bcl-xl,
Bcl-w) and the pro-apoptotic (Bax, Bak, Bid). The balance between the pro-apoptotic and anti-apoptotic proteins determines
cell survival or death. We discuss recent findings in the molecular mechanisms of UV induced apoptosis.
Keywords
apoptosis; UV radiation; UV skin damage
Hrčak ID:
72305
URI
Publication date:
25.9.2011.
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