UVB-Response in Human Skin
& Its Modulation by the Proto-
Oncogenic AKT Signaling Pathway

By David Decraene
September 2004
Leuven University Press
ISBN: 9058673863
142 pages, Illustrated, 6 " x 9 "
$87.50 Paper Original


This is a Ph.D. dissertation. The sun emits a wide spectrum of electromagnetic waves. Fortunately, most of the harmful high energy radiation is filtered out by our planet's atmosphere and the ozone layer. One exception lies within the Ultraviolet region of the spectrum (200-400nm) reaches the earth's surface and penetrates human skin.

This small fraction of the solar spectrum is responsible for nearly all of the adverse effects of sunlight to mankind, including sunburn, immunosuppression, photodamage of the dermal connective tissue and photoaging. Most importantly, Ultraviolet radiation turns sunlight into the major cause of human skin cancer. The UVB-fraction, the most energetic fraction of solar radiation that reaches earth's surface, exerts its adverse effects through both oxidative stress and direct DNA damage.

UVB produces some amount of reactive oxygen species (ROS) through interaction with endogenous photosensitizers. These ROS can in turn damage DNA, proteins and membranes. They are involved in Photodamage of the dermal connective tissue, characteristic for photoaging, through direct damage to connective tissue cells and proteins and through the induction of proteolytic pathways. The extent to which ROS participates in the UVB-response is however still an area of debate.

Contents include: Introduction, IGF-1 mediated AKT activation postpones the onset of UVB-induced apoptosis, providing more time for cyclobutane thymine dimer removal in primary human keratinocytes, AKT status controls susceptibility of malignant keratinocytes to the early-activated and UVB-induced apoptotic pathway, A role for IGF-1/AKT induced BAD translocation in the inhibition of the early-activated apoptotic pathway in UVB-irradiated Keratinocytes, A synthetic superoxide dismutase/catalase-mimetic (EUK-134) inhibits membrane damage-induced activation of MAPK pathways and reduces p53 accumulation in UVB-exposed primary human keratinocytes, The UVB-response in human skin and its modulation by the AKT kinase pathway, Summary.

Dermatology; Oncology
Acta Biomedica Lovaniensia No. 315

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