Independent contribution of three different pathways to ultraviolet-B-induced apoptosis

Ultraviolet-B radiation (UVB) causes a variety of biological effects which include the induction of apoptosis. UVB-induced apoptosis provides a well controlled scavenging mechanism protecting cells from malignant transformation. To induce programmed cell death, UVB uses a variety of cellular signaling pathways. In this context induction of nuclear DNA damage seems to be the predominant pathway, since experimental reduction of DNA damage was associated with a strong suppression of apoptosis. Additionally, UVB has been shown to target cytoplasmatically located or membrane bound components to induce signal transduction. UVB was found to directly activate cell surface death receptors, thereby triggering the apoptotic machinery. Furthermore, UVB-induced intracellular formation of reactive oxygen species (ROS) accompanied by mitochondrial dysfunction and cytochrome c release was demonstrated to be additionally involved in the apoptotic program. The following review will briefly discuss current aspects of the interplay between the different signaling pathways involved in UVB-induced apoptosis.