Involvement of growth factor receptors in the mammalian UVC response

Sachsenmaier, Christoph; Radler‐Pohl, Adriana; Zinck, Raymund; Nordheim, Alfred; Herrlich, Peter; Rahmsdorf, Hans J.

doi:10.1016/0092-8674(94)90272-0

Cited by 433 publications

(362 citation statements)

References 46 publications

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“…Initially described as a pathway that was unresponsive to or downregulated by stress stimuli, it is now clear that oxidative stress leads to substantial activation of ERK and that growth factor receptors play an important role in mediating this effect. A number of growth factor receptors including the epidermal growth factor (EGF) receptor, plateletderived growth factor (PDGF) receptor, and the T-cell receptor complex have been shown to undergo phosphorylation in response to oxidative insults such as hydrogen peroxide, asbestos, short wave ultraviolet light (UVC) irradiation and arsenite, and interference of these phosphorylations attenuates ERK activation in response to oxidative stress (Sachsenmaier et al, 1994;Schieven et al, 1994;Huang et al, 1996;Knebel et al, 1996;Zanella et al, 1996;Chen et al, 1998). Likewise, expression of inactive mutant forms of various growth factor receptors reduces activation of ERK by oxidative stress (Sachsenmaier et al, 1994), while overexpression of certain normal growth factor receptors, such as the Trk receptor for nerve growth factor in rat PC12 cells, results in enhanced activation of ERK by hydrogen peroxide (Guyton et al, 1998).…”

Section: Erk Pathwaymentioning

confidence: 99%

Cellular response to oxidative stress: Signaling for suicide and survival*

Martindale

Holbrook

2002

Journal Cellular Physiology

2,100

1,596

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Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of many diseases as well as to degenerative processes of aging has becoming increasingly apparent over the past few years. Cells contain a number of antioxidant defenses to minimize fluctuations in ROS, but ROS generation often exceeds the cell's antioxidant capacity, resulting in a condition termed oxidative stress. Host survival depends upon the ability of cells and tissues to adapt to or resist the stress, and repair or remove damaged molecules or cells. Numerous stress response mechanisms have evolved for these purposes, and they are rapidly activated in response to oxidative insults. Some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death. Still others have been implicated in both extremes depending on the particular circumstances. In this review, we discuss the various signaling pathways known to be activated in response to oxidative stress in mammalian cells, the mechanisms leading to their activation, and their roles in influencing cell survival. These pathways constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or attenuating its sequelae. Published 2002 Wiley‐Liss, Inc.

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Section: Erk Pathwaymentioning

confidence: 99%

Cellular response to oxidative stress: Signaling for suicide and survival*

Martindale

Holbrook

2002

Journal Cellular Physiology

2,100

1,596

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“…UV light induces ligand-independent activation of various receptors, receptor tyrosine kinases, and protein tyrosine kinases at the inner side of the plasma membrane (36)(37)(38)(39)(40). Recently, UV light was found to cause epidermal and plateletderived growth factor receptor autophosphorylation by inhibiting dephosphorylation of these receptors, presumably by targeting membrane-associated protein tyrosine phosphatases (41).…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of interferon γ-activated STAT1 by UV light

Aragane¹,

Kulms²,

Luger³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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STAT1 is a cytoplasmic transcription factor that is phosphorylated by Janus kinases (Jak) in response to interferon-␥ (IFN␥). Phosphorylated STAT1 translocates to the nucleus, where it turns on specific sets of IFN␥-inducible genes. Here, we show that UV light interferes with tyrosine phosphorylation of STAT1, thereby hindering IFN␥ from exerting its biological effects. This effect is not due to a down-regulation of the IFN␥ receptor because phosphorylation of upstream-located Jak1 and Jak2 was not suppressed by UV light. In contrast, UV light had no effect on the phosphorylation of STAT3, which is activated by the proinf lammatory cytokine interleukin 6. The UV light effect on STAT1 phosphorylation could be antagonized by vanadate, indicating at least partial involvement of a protein tyrosine phosphatase. Therefore, this study indicates a mechanism by which UV light can inhibit gene activation and suggests STAT1 as a new extranuclear UV target closely located to the membrane.

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“…MAP kinase families, that include extracellular regulated kinase (ERK) 1, 2, p38, and stress-activated protein kinase/c-Jun N-terminal kinase (JNK), are essential signal transduction components, and are involved in various stimulatory or inhibitory signals [12][13][14][15][16]. The ERK is activated by various growth factors and phorbol esters, but are only weakly activated by inflammatory cytokines (tumor necrotic factor-α, interlleukin-1) and environmental stress.…”

Section: Ultraviolet (Uv) B Irradiation Induces Various Effects On Kementioning

confidence: 99%

Differential phosphorylation of mitogen-activated protein kinase families by epidermal growth factor and ultraviolet B irradiation in SV40-transformed human keratinocytes

Takahashi

Kinouchi

Manabe

et al. 2001

Journal of Dermatological Science

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ELSEVIER, Nakamura, S; Takahashi, H; Kinouchi, M; Manabe, A; Ishida-Yamamoto, A; Hashimoto, Y; Iizuka, H, JOURNAL OF DERMATOLOGICAL SCIENCE, 25(2), 139-149, 2001. authorSV-40 transformed human keratinocytes (SVHK cells) were stimulated with epidermal growth factor (EGF)2 and ultraviolet B (UVB) irradiation. Following the stimulation, cell growth, apoptosis, and the activities of mitogen-activated protein (MAP) kinase families were analyzed. EGF (100ng/ml) increased SVHK cell number compared with control cells cultured in serum-free DMEM medium. The EGF-stimulated cells did not show DNA fragmentation. In contrast, UVB irradiation (40mJ/cm2) markedly decreased viable cell number, that was accompanied with DNA fragmentation. EGF stimulated extracellular signal-regulated kinase (ERK) and stress-activated protein kinase/c-Jun N-terminal kinase (JNK). Following the EGF stimulation, phosphorylated ERK and JNK were detected by phospho-p42/44 MAP kinase antibody and phospho-SAPK/JNK antibody, respectively. On the other hand, UVB irradiation stimulated the phosphorylation of p38 and JNK but not of ERK. The stimulation of ERK and JNK induced by EGF was observed earlier than the stimulation of p38 and JNK induced by UVB. PD98059, a specific MAP kinase kinase (MAPKK) 1 (also referred to as MEK1) inhibitor, inhibited EGF-dependent cell proliferation, that was associated with the inhibition of ERK and JNK phosphorylation. In contrast, UVB-induced overall cell death was not significantly affected by PD98059, that inhibited phosphorylation of JNK but not of p38. PD98059, however, significantly augmented UVB-induced cell death earlier time points (30min - 2 h). These results indicate that ERK and JNK are activated following EGF stimulation, that might be associated with cell proliferation. On the other hand, UVB-induced apoptosis seems to be mostly associated with the activation of p38. JNK stimulation might provide an anti-apoptotic tonus during the UVB-induced, p38-associated SVHK cell death

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Involvement of growth factor receptors in the mammalian UVC response

Cited by 433 publications

References 46 publications

Cellular response to oxidative stress: Signaling for suicide and survival*

Cellular response to oxidative stress: Signaling for suicide and survival*

Down-regulation of interferon γ-activated STAT1 by UV light

Differential phosphorylation of mitogen-activated protein kinase families by epidermal growth factor and ultraviolet B irradiation in SV40-transformed human keratinocytes

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