Title: Differential stimulation of ERK and JNK activities by ultraviolet B irradiation and epidermal growth factor in human keratinocytes
Authors: Assefa, Z ×
Garmyn, Maria
Bouillon, Roger
Merlevede, Wilfried
Vandenheede, Jackie
Agostinis, Patrizia #
Issue Date: Jun-1997
Publisher: Blackwell science inc
Series Title: Journal of Investigative Dermatology vol:108 issue:6 pages:886-891
Abstract: Exposure of mammalian cells to solar ultraviolet (UV) radiation leads to the expression of several genes, and UV has been recognized as a major initiator and promoter of skin cancer. The component of the solar radiation that contributes most to human skin malignancy is UVB (280-320 nm) and, to a lesser extent, UVA (320-400 nm), whereas the high-energy UVC (100-280 nm) is absorbed by the earth's upper atmosphere. Sublethal doses of UVB produce strong induction of c-jun and c-fos transcripts in several cells including human primary keratinocytes. The present report confirms that this is also the case in the HaCaT cell line and shows that similar UVB doses are potent inducers of the JNK/SAPK family of mitogen-activated protein kinases but only weak activators of ERKs. Epidermal growth factor (EGF) caused rapid induction of both JNK- and ERK-signaling pathways, and the downmodulation of the EGF-signaling pathway by EGF pre-treatment inhibited the UVB-induced JNK1 activation. Prior UVB irradiation of the cells decreased the level of the ERK2 activation by a subsequent EGF treatment, but this sensitized the cells and allowed for the super-activation of JNK1 after a rechallenge with either UVB or EGF. The antioxidant N-acetylcysteine impaired the UVB- and EGF-induced activation of JNK1. Our data suggest the presence of shared signaling component(s) in the UVB- and EGF-induced cellular response pathways and imply that oxidative stress plays a significant role in the activation of JNK1 by UVB and EGF.
ISSN: 0022-202X
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Dermatology
Clinical and Experimental Endocrinology
Biochemistry Section (Medicine) (-)
Laboratory of Protein Phosphorylation and Proteomics
Laboratory of Cell Death Research & Therapy
× corresponding author
# (joint) last author

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