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• W2089432885 abstract "extracellular signal-regulated kinase c-Jun N-terminal kinase mitogen-activated protein kinase ultraviolet To the Editor: The molecular response mechanisms and signaling pathways activated upon exposure to ultraviolet (UV) radiation have been extensively studied within the last two decades (for a review seeBrenneisen et al., 2002Brenneisen P. Sies H. Scharffetter-Kochanek K. Ultraviolet-B irradiation and matrix metalloproteinases: From induction via signaling to initial events.Ann N Y Acad Sci. 2002; 973: 31-43Crossref PubMed Scopus (339) Google Scholar; Bode and Dong, 2003Bode A.M. Dong Z. Mitogen-activated protein kinase activation in UV-induced signal transduction.Sci STKE 2003. 2003; RE2Google Scholar). Although many signaling pathways can be activated by both UVA as well as UVB, there are several distinctions indicating wavelength-specific response patterns accommodated by the terms UVA response and UVB response. The role of three mitogen-activated protein kinase (MAPK) pathways in these responses, central regulators of multiple cellular functions, has been studied extensively: (i) the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, activated primarily by growth factors upon binding to tyrosine kinase receptors as well as reactive oxygen species (ROS), (ii) the c-Jun N-terminal kinase (JNK), and (iii) p38 pathways also termed stress-activated protein kinases (SAPK), predominantly induced by inflammatory cytokines and environmental stressors such as ROS, heat, and osmotic shock. Activation of MAPK signaling pathways upon exposure to UV radiation has been demonstrated in a number of different cell lines and in human skin in vivo (Bode and Dong, 2003Bode A.M. Dong Z. Mitogen-activated protein kinase activation in UV-induced signal transduction.Sci STKE 2003. 2003; RE2Google Scholar). Given that human skin is primarily exposed to UV light from solar radiation consisting of both UVA and UVB, we sought to explore a potential interaction between the distinct UVA and UVB responses at the level of MAPK. First, we determined the MAPK activation pattern elicited by either UVA or UVB radiation alone in cultured primary human keratinocytes (Figure 1a and b). Irradiation of keratinocytes with UVA (30 J per cm2) resulted in a modest and transient activation of ERK1/2 15–30 min after UVA exposure, whereas UVB irradiation (100 J per m2) resulted in a strong and immediate ERK1/2 phosphorylation that sustained up to 60 min after irradiation. Only a minor activation of the stress-activated protein kinases, p38MAPK and JNK1/2, was detected after both UVA and UVB irradiation. The irradiation doses chosen in these experiments were previously found to be optimal in triggering UV signaling responses in human keratinocytes without induction of apoptosis and necrosis (Krutmann and Grewe, 1995Krutmann J. Grewe M. Involvement of cytokines, DNA damage, and reactive oxygen intermediates in ultraviolet radiation-induced modulation of intercellular adhesion molecule-1 expression.J Invest Dermatol. 1995; 105: 67S-70SCrossref PubMed Scopus (107) Google Scholar; Grether-Beck et al., 2000Grether-Beck S. Bonizzi G. Schmitt-Brenden H. et al.Non-enzymatic triggering of the ceramide signalling cascade by solar UVA radiation.EMBO J. 2000; 19: 5793-5800Crossref PubMed Scopus (93) Google Scholar). We next asked whether any crosstalk may occur between the activated signaling pathways involved in the UVA- or UVB-induced stress response. To determine whether such an interaction exists, we exposed human epidermal keratinocytes sequentially to UVA and UVB radiation. Cells were irradiated with UVA followed by immediate exposure to UVB. The UVB-induced MAPK activation pattern after preirradiation with UVA differed notably from that induced by UVB alone (Figure 1c). The strong phosphorylation of ERK1/2 was prevented, whereas p38 and JNK phosphorylation were enhanced by UVA preirradiation. Sequential exposure to UVA followed by UVB led to an attenuation of ERK phosphorylation falling significantly below that in UVB-irradiated cells 30–60 min after irradiation. On the other hand, phosphorylation of p38 and JNK was increased markedly 30–60 min after UV exposure (Figure 1c). To further understand this signaling crosstalk between UVA- and UVB-induced MAPK activation, the sequence of irradiation was changed, i.e. UVB irradiation was followed by UVA exposure (Figure 1d). Interestingly, reversing the sequence of irradiation produced changes similar to the UVA/UVB-induced MAPK activation pattern: ERK phosphorylation was significantly reduced 45–60 min after exposure, but phosphorylation of p38MAPK and JNK1/2 was enhanced. Thus, the observed crosstalk pattern of MAPK activation by irradiation with UVA and UVB seems to be independent of the sequence of irradiation. These results lend support to the initial hypothesis that the two distinct stress responses elicited by UVA or UVB interact with each other, producing a “third” response that is different from either alone and cannot be explained by a simple addition of effects. Regarding the UVA-induced attenuation of ERK signaling, these results are consistent with previously published studies. We and others have demonstrated that 1O2 or UVA radiation interferes with the epidermal growth factor receptor (EGFR)/ERK1/2 signaling pathway. Binding of EGF to and subsequent activation of the EGFR, ERK1/2, and transcription factors such as Activator Protein-1, nuclear factor κ B, and STAT1 is impaired upon irradiation with UVA (Maziere et al., 2003Maziere C. Floret S. Santus R. Morliere P. Marcheux V. Maziere J.C. Impairment of the EGF signaling pathway by the oxidative stress generated with UVA.Free Radic Biol Med. 2003; 34: 629-636Crossref PubMed Scopus (39) Google Scholar).He et al., 2003He Y.Y. Huang J.L. Gentry J.B. Chignell C.F. Epidermal growth factor receptor down-regulation induced by UVA in human keratinocytes does not require the receptor kinase activity.J Biol Chem. 2003; 278: 42457-42465Crossref PubMed Scopus (42) Google Scholar) described a UVA-induced downregulation of the EGFR. In addition, singlet oxygen has been shown to induce a loss of EGFR and attenuation of basal and EGF- or PDGF-induced activation of growth factor signaling pathways (Zhuang et al., 2003Zhuang S. Ouedraogo G.D. Kochevar I.E. Downregulation of epidermal growth factor receptor signaling by singlet oxygen through activation of caspase-3 and protein phosphatases.Oncogene. 2003; 22: 4413-4424Crossref PubMed Scopus (42) Google Scholar; Schieke et al., 2004Schieke S.M. Von Montfort C. Buchczyk D.P. et al.Singlet oxygen-induced attenuation of growth factor signaling: Possible role of ceramides.Free Radic Res. 2004; 38: 729-737Crossref PubMed Scopus (40) Google Scholar). Taken together, these results show that UVA/singlet oxygen generally interfere with growth factor signaling cascades, e.g. EGFR/ERK1/2, activation of which is also part of the keratinocyte stress response to UVB radiation (Peus et al., 1999Peus D. Meves A. Vasa R.A. Beyerle A. O'Brien T. Pittelkow M.R. H2O2 is required for UVB-induced EGF receptor and downstream signaling pathway activation.Free Radic Biol Med. 1999; 27: 1197-1202Crossref PubMed Scopus (78) Google Scholar). Over the last several years, remarkable progress has been made in understanding the signaling pathways and mechanisms regulating the cellular response to UV radiation. Analysis of these pathways has shown wavelength-specific differences in the response to UV radiation and despite some overlap, distinct UVA and UVB response mechanisms have been characterized. Given that skin cells such as epidermal keratinocytes are naturally exposed to both UVA and UVB radiation, it is conceivable that interactions between the different response mechanisms exist. Here, the molecular crosstalk between UVA and UVB signaling at the level of MAPK represents one such interaction in an evolutionarily conserved signaling pathway regulating a variety of diverse biological processes such as proliferation, cell death, and senescence. Our results suggest that skin cells have developed elaborate molecular defense strategies in order to respond to solar radiation stress that go beyond a mere additive effect of their single components, i.e. UVA and UVB responses. The observed crosstalk at the level of MAPK might provide new insights into the previously reported contradictory effects of combined UVA and UVB irradiation in immune function: UVA has been demonstrated to protect against UVB-induced immunosuppression (Reeve and Tyrrell, 1999Reeve V.E. Tyrrell R.M. Heme oxygenase induction mediates the photoimmunoprotective activity of UVA radiation in the mouse.Proc Natl Acad Sci USA. 1999; 96: 9317-9321Crossref PubMed Scopus (98) Google Scholar; Allanson and Reeve, 2004Allanson M. Reeve V.E. Immunoprotective UVA (320–400 nm) irradiation upregulates heme oxygenase-1 in the dermis and epidermis of hairless mouse skin.J Invest Dermatol. 2004; 122: 1030-1036Abstract Full Text Full Text PDF PubMed Scopus (41) Google Scholar) as well as to augment solar radiation-induced immunosuppression (Kuchel et al., 2002Kuchel J.M. Barnetson R.S. Halliday G.M. Ultraviolet A augments solar-simulated ultraviolet radiation-induced local suppression of recall responses in humans.J Invest Dermatol. 2002; 118: 1032-1037Crossref PubMed Scopus (39) Google Scholar). But, the functional consequences of the crosstalk at the transcriptional level need to be characterized, and many questions remain regarding the effects of this interaction on photoaging and photocarcinogenesis. In addition, further analysis of this crosstalk will aid in the evaluation of photoprotective strategies with important implications for the development of modern broad-band sunscreens. These studies were supported by a grant from the Deutsche Forschungsgemeinschaft SFB 503, Project B2." @default.
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• W2089432885 title "Molecular Crosstalk of the Ultraviolet A and Ultraviolet B Signaling Responses at the Level of Mitogen-Activated Protein Kinases" @default.
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