Epidermal Growth Factor Receptor Is a Critical Mediator of Ultraviolet B Irradiation-Induced Signal Transduction in Immortalized Human Keratinocyte HaCaT Cells

Xu, Yuntao; Voorhees, John J.; Fisher, Gary J.

doi:10.2353/ajpath.2006.050449

Cited by 63 publications

(60 citation statements)

References 66 publications

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“…Although the consequences of the cellular stress response after UV irradiation are well described (1-3, 36, 37), the chromophore for UV that initiates cell surface receptor and subsequent MAPK activation has so far been inscrutable (38). It has previously been proposed that parts of the EGFR activation are mediated by UVB-induced reactive oxygen species, which directly inhibit protein tyrosine phosphatase activities (39).…”

Section: Discussionmentioning

confidence: 99%

Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation

Fritsche

Schäfer

Calles

et al. 2007

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

404

405

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UVB radiation-induced signaling in mammalian cells involves two major pathways: one that is initiated through the generation of DNA photoproducts in the nucleus and a second one that occurs independently of DNA damage and is characterized by cell surface receptor activation. The chromophore for the latter one has been unknown. Here, we report that the UVB response involves tryptophan as a chromophore. We show that through the intracellular generation of photoproducts, such as the arylhydrocarbon receptor (

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Section: Discussionmentioning

confidence: 99%

Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation

Fritsche

Schäfer

Calles

et al. 2007

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

404

405

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“…In cultured skin keratinocytes (HaCaT cell line), EGFR, among three of these cell surface receptors, plays a preeminent role in UV irradiation-induced activation of multiple signal transduction pathways, including MAPK, AKT and PKC [31]. This finding suggests that interconnections among cell surface receptor activation and downstream signaling pathways that are triggered in response to UV irradiation may differ depending on cell type and cellular context.…”

Section: Discussionmentioning

confidence: 87%

EGFR activation confers protections against UV-induced apoptosis in cultured mouse skin dendritic cells

Cao

Lü

Jiang

et al. 2008

Cellular Signalling

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Ultraviolet radiation (UV) induces apoptosis and functional maturation in skin dendritic cells (DCs). However, the molecular mechanisms through which UV activates DCs have not been thoroughly investigated. In this study, we examined the mechanisms of activation and apoptosis of DC after UV irradiation by focusing on epidermal growth factor receptor (EGFR). Our previous studies have demonstrated that in addition to cognate ligands, EGFR is also activated by UVB irradiation in cultured human skin keratinocytes in vitro and in human skin in vivo. We found for the first time in this study that UV also induces EGFR activation in cultured mouse skin DCs (XS 106 cell line) as well as mouse monocyte-derived dendritic cells (MoDCs). Pharmacological inhibition of EGFR tyrosine kinase significantly inhibits UV-induced ERK, p38, and JNK MAP kinases, and their effectors, transcription factors c-Fos and c-Jun. Inhibition of EGFR also suppresses UV-induced activation of PI3K/AKT/mTOR/S6K and NF-κB signal transduction pathways. Our data demonstrated that UV induces LKB1/AMPK pathway, also dependent on EGFR trans-activation. We further observed that MAPK, LKB1/AMPK, PI3K/AKT/mTOR/S6K as well as NF-κB activation are impaired in EGFR−/− cells compared to wide type MEF cells after UV radiation. Taken together, we conclude that UV induces multiple signaling pathways mediated by EGFR trans-activation leading to possible maturation, apoptosis and survival, and EGFR activation protects against UVinduced apoptosis in cultured mouse dendritic cells.

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“…The latest research by Xu et al (2006) shows that UVB irradiation of immortalized keratinocytes can increase c-jun and c-fos expression, while this trend can be significantly reduced by Egfr antagonists. This strongly indicates that Egfr plays an important role in skin aging.…”

Section: Discussionmentioning

confidence: 99%

Effect of atmospheric fine particles on epidermal growth factor receptor mRNA expression in mouse skin tissue

Han

Zhang

et al. 2016

Genet. Mol. Res.

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ABSTRACT.We investigated the effect of atmospheric fine particles on epidermal growth factor receptor (Egfr) mRNA expression in mouse skin tissue and explored the effect of atmospheric fine particles on skin aging. Forty female BALB/c mice were randomly divided into four groups (each comprising 10 mice) as follows: a saline control group and low-, medium-, and high-dose atmospheric fine particle groups (1.6, 8.0, and 40.0 mg/kg, respectively) (fine particles were defined as those with a diameter of ≤2.5 μm, i.e., PM2.5). Each dose group was exposed to intratracheal instillation for 3 days. Twenty-four hours after the last exposure, real-time quantitative polymerase chain reaction was used to detect the expression of Egfr mRNA in the skin tissue of each mouse. The expression levels of Egfr mRNA in the medium-and high-dose PM2.5 groups were significantly higher (P < 0.05) than that in the control group, and were positively correlated with the dose. Medium and high concentrations of PM2.5 can induce the expression of Egfr mRNA and promote skin aging.

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Epidermal Growth Factor Receptor Is a Critical Mediator of Ultraviolet B Irradiation-Induced Signal Transduction in Immortalized Human Keratinocyte HaCaT Cells

Cited by 63 publications

References 66 publications

Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation

Lightening up the UV response by identification of the arylhydrocarbon receptor as a cytoplasmatic target for ultraviolet B radiation

EGFR activation confers protections against UV-induced apoptosis in cultured mouse skin dendritic cells

Effect of atmospheric fine particles on epidermal growth factor receptor mRNA expression in mouse skin tissue

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