H2O2 is required for UVB-induced EGF receptor and downstream signaling pathway activation

Péus, Dominik; Meves, Alexander; Vasa, R; Beyerle, Astrid; O’Brien, Timothy J.; Pittelkow, Mark R.

doi:10.1016/s0891-5849(99)00198-7

Cited by 78 publications

(63 citation statements)

References 23 publications

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“…Cell lysates were subjected to be analyzed by Western blotting. All results shown above are the representatives from three to four independent experiments.ECG inhibits8 H 2 O 2 -induced ERK1/2, JNK andp38 activation It has been reported that H 2 O 2 is required for UVB-induced activation of the EGF receptor and downstream signaling pathway(s) [28]. Moreover, several studies demonstrated that H 2 O 2 treatment induces phosphorylation of MAPKs in keratinocytes [17], suggesting that it causes an oxidative stress on skin cells.…”

Section: Ecg Inhibits Uvb-induced Erk1/2 Jnk Andp38 Activationmentioning

confidence: 98%

“…Hydrogen peroxide is generated in cultured human skin cells during UVB irradiation [17,28]. We therefore suspected that ECG affected UVB-induced intracellular H 2 O 2 production.…”

Section: Ecg Inhibits Uvb-induced H 2 O 2 Generation In Keratinocytesmentioning

confidence: 99%

“…Moreover, ECG inhibited H 2 O 2 -induced MAPKs activation. It has been shown that UVB-induced ROS formation is responsible for the activation of MAPKs [28]. Therefore, exogenous H 2 O 2 may directly activate MAPKs signaling pathway through penetrate cell membrane.…”

Section: Ecg Inhibits Uvb-induced Erk1/2 Jnk Andp38 Activationmentioning

confidence: 99%

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(-)-Epicatechin-3-gallate, a Green Tea Polyphenol Is a Potent Agent Against UVB-induced Damage in HaCaT Keratinocytes

Fang

Chiang

et al. 2007

Molecules

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(-)-Epicatechin-3-gallate (ECG) is a polyphenolic compound similar to (-)-epigallocatechin-3-gallate (EGCG) which is abundant in green tea. Numerous workers have proposed that EGCG protects epidermal cells against UVB-induced damage. However, little has been known about whether ECG protects keratinocytes against UVB-induced damage. We decided to investigate the protective effects and underlying mechanisms of ECG on UVB-induced damage. Cell viability was determined by the MTT assay. Activation of ERK1/2, p38 and JNK was analyzed by Western blotting. Intracellular H 2 O 2 production and DNA content was analyzed by flow cytometry. Lipid peroxidation was assayed by colorimetry. In our study, we found that ECG dose-dependently attenuated UVB-induced keratinocyte death. Moreover, ECG markedly inhibited UVB-induced cell membrane lipid peroxidation and H 2 O 2 generation in keratinocytes, suggesting that ECG can act as a free radical scavenger when keratinocytes were photodamaged. In parallel, H 2 O 2 -induced the activation of ERK1/2, p38 and JNK in keratinocytes could be inhibited by ECG. UVB-induced pre-G 1 arrest leading to apoptotic changes of keratinocytes were blocked by ECG. Taken together, we provide here evidence that ECG protects keratinocytes from Molecules 2007, 12 1846 UVB-induced photodamage and H 2 O 2 -induced oxidative stress, possibly through inhibition of the activation of ERK1/2, p38 and JNK and/or scavenging of free radicals.

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Section: Ecg Inhibits Uvb-induced Erk1/2 Jnk Andp38 Activationmentioning

confidence: 98%

“…Hydrogen peroxide is generated in cultured human skin cells during UVB irradiation [17,28]. We therefore suspected that ECG affected UVB-induced intracellular H 2 O 2 production.…”

Section: Ecg Inhibits Uvb-induced H 2 O 2 Generation In Keratinocytesmentioning

confidence: 99%

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(-)-Epicatechin-3-gallate, a Green Tea Polyphenol Is a Potent Agent Against UVB-induced Damage in HaCaT Keratinocytes

Fang

Chiang

et al. 2007

Molecules

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“…An intact Txn system may be necessary to attenuate signaling by surface receptors. In response to ligand binding, NADPH-oxidase enzymes associated with the cytosolic aspect of growth factor receptors generate H 2 O 2 [22][23][24]26,[75][76][77][78][79][80][81][82][83]. A conserved catalytic cysteine at the active site of protein tyrosine phosphatases is oxidized by H 2 O 2 to a sulfenic acid, which further reacts with a backbone nitrogen to form a sulfenylamide [68].…”

Section: Effects On Signalingmentioning

confidence: 99%

Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome

Bondareva¹,

Capecchi²,

Iverson³

et al. 2007

Free Radical Biology and Medicine

102

115

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Thioredoxin reductases (Txnrd)1 maintain intracellular redox homeostasis in most organisms. Metazoans Txnrds also participate in signal transduction. Mouse embryos homozygous for a targeted null mutation of the txnrd1 gene, encoding the cytosolic thioredoxin reductase, were viable at embryonic day 8.5 (E8.5) but not at E9.5. Histology revealed that txnrd1 −/− cells were capable of proliferation and differentiation; however, mutant embryos were smaller than wild-type littermates and failed to gastrulate. In situ marker gene analyses indicated primitive streak mesoderm did not form. Microarray analyses on E7.5 txnrd −/− and txnrd +/+ littermates showed similar mRNA levels for peroxiredoxins, glutathione reductases, mitochondrial Txnrd2, and most markers of cell proliferation. Conversely, mRNAs encoding sulfiredoxin, IGF-binding protein 1, carbonyl reductase 3, glutamate cysteine ligase, glutathione S-transferases, and metallothioneins were more abundant in mutants. Many gene expression responses mirrored those in thioredoxin reductase 1-null yeast; however mice exhibited a novel response within the peroxiredoxin catalytic cycle. Thus, whereas yeast induce peroxiredoxin mRNAs in response to thioredoxin reductase disruption, mice induced sulfiredoxin mRNA. In summary, Txnrd1 was required for correct patterning of the early embryo and progression to later development. Conserved responses to Txnrd1 disruption likely allowed proliferation and limited differentiation of the mutant embryo cells.

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“…It has been suggested that p38 MAPK and PI3K activation are mediated in part through ligand-independent activation of the epidermal growth factor receptor, which is dependent on generation of reactive oxygen species (49)(50)(51). Activation of the epidermal growth factor receptor by UVB in this ligand-independent manner leads to Ras and RAC activation, which in turn induces reactive oxygen species through the activation of NADPH oxidase by RAC.…”

Section: Sb202190 and Ly294002 Inhibit Ap-1 Activation And Cox-2 Exprmentioning

confidence: 99%

Inhibition of p38 Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase Decreases UVB-Induced Activator Protein-1 and Cyclooxygenase-2 in a SKH-1 Hairless Mouse Model

Bachelor

Cooper

Sikorski

et al. 2005

Molecular Cancer Research

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Activation of activator protein-1 (AP-1) and increased expression of cyclooxygenase-2 (COX-2) have been clearly shown to play a functional role in UVB-induced skin tumor promotion. In this study, we examined UVB-induced signal transduction pathways in SKH-1 mouse epidermis leading to increases in COX-2 expression and AP-1 activity. We observed rapid increases in p38 mitogen-activated protein kinase (MAPK) signaling through activation of p38 MAPK and its downstream target, MAPK activated protein kinase-2. UVB also increased phosphatidylinositol 3-kinase (PI3K) signaling as observed through increases in AKT and GSK-3B B phosphorylation. Activation of the p38 MAPK and PI3K pathways results in the phosphorylation of cyclic AMP -responsive element binding protein, which was also observed in UVB-irradiated SKH-1 mice. Topical treatment with SB202190 (a specific inhibitor of p38 MAPK) or LY294002 (a specific inhibitor of PI3K) significantly decreased UVB-induced AP-1 activation by 84% and 68%, respectively, as well as COX-2 expression. Our data show that in mouse epidermis, UVB activation of the p38 MAPK and PI3K pathways leads to AP-1 activation and COX-2 expression. (Mol Cancer Res 2005;3(2):90 -9)

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H2O2 is required for UVB-induced EGF receptor and downstream signaling pathway activation

Cited by 78 publications

References 23 publications

(-)-Epicatechin-3-gallate, a Green Tea Polyphenol Is a Potent Agent Against UVB-induced Damage in HaCaT Keratinocytes

(-)-Epicatechin-3-gallate, a Green Tea Polyphenol Is a Potent Agent Against UVB-induced Damage in HaCaT Keratinocytes

Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome

Inhibition of p38 Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase Decreases UVB-Induced Activator Protein-1 and Cyclooxygenase-2 in a SKH-1 Hairless Mouse Model

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