Essential role of Nrf2 in keratinocyte protection from UVA by quercetin

Kimura, Shintarou; Warabi, Eiji; Yanagawa, Toru; Ma, Deying; Itoh, Ken; Ishii, Yoshiyuki; Kawachi, Yasuhiro; Ishii, Tetsuro

doi:10.1016/j.bbrc.2009.06.136

Cited by 78 publications

(61 citation statements)

References 31 publications

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“…Further, cells sensitized to Nrf2 suffered more UVA irradiationmediated cell damage, as demonstrated by a decrease in cell viability and increase in the release of LDH. This supports the notion that Nrf2 plays a role in protecting both skin keratinocytes and fibroblasts from exposure to UVA irradiation (10,11).…”

supporting

confidence: 78%

“…A study by Hirota and a previous study by the current authors also showed that UVA irradiation causes nuclear accumulation of Nrf2 in human and ) to moderate (250 kJ•m −2 ) doses of UVA irradiation (9,10). Nrf2 may be involved in protection of HaCaT human skin keratinocytes from UVA irradiation by quercetin, an antioxidant (11). Therefore, increased cellular antioxidant or detoxification capacity as a result of increased Nrf2 levels may help with cellular defense.…”

Section: Introductionsupporting

confidence: 67%

“…Cells were grown on 6-well plates for 48 h and collected and then Nrf2 levels were analyzed using Western blotting. cells against oxidative stress, which includes UVA irradiation-induced damage (10,11). A moderate to high dose (400 kJ•m −2 ) of UVA irradiation slightly increased Nrf2 protein levels, although not significantly, and immunostaining also revealed that Nrf2 accumulated only slightly in the nucleus following this dose of UVA irradiation, the same as happens at 250 kJ•m − 2 (14) and 500 kJ•m −2 (data not shown).…”

mentioning

confidence: 76%

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Nrf2-mediated protection against UVA radiation in human skin keratinocytes

Tian

Zhang

Lai

et al. 2011

BST

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supporting

confidence: 78%

Section: Introductionsupporting

confidence: 67%

mentioning

confidence: 76%

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Nrf2-mediated protection against UVA radiation in human skin keratinocytes

Tian

Zhang

Lai

et al. 2011

BST

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“…Multiple components of coffee have been shown to induce Nrf2 activation, including cafestol and kahweol (Higgins et al 2008), and cafestol is protective in the Drosophila PD models (Trinh et al 2010). A number of natural polyphenols, including hydroxytyrosol (Martin et al 2010), quercetin (Kimura et al 2009), and epigallocatechin-3-gallate (Na et al 2008), have also been shown to activate the Nrf2 pathway. These observations suggest that the skn-1/Nrf2 pathway has evolved to be broadly responsive to xenobiotic compounds, and that there may be multiple compounds in coffee extracts that contribute to activation of this pathway.…”

Section: Resultsmentioning

confidence: 99%

Genetic Mechanisms of Coffee Extract Protection in aCaenorhabditis elegansModel of β-Amyloid Peptide Toxicity

2010

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Epidemiological studies have reported that coffee and/or caffeine consumption may reduce Alzheimer's disease (AD) risk. We found that coffee extracts can similarly protect against b-amyloid peptide (Ab) toxicity in a transgenic Caenorhabditis elegans Alzheimer's disease model. The primary protective component(s) in this model is not caffeine, although caffeine by itself can show moderate protection. Coffee exposure did not decrease Ab transgene expression and did not need to be present during Ab induction to convey protection, suggesting that coffee exposure protection might act by activating a protective pathway. By screening the effects of coffee on a series of transgenic C. elegans stress reporter strains, we identified activation of the skn-1 (Nrf2 in mammals) transcription factor as a potential mechanism of coffee extract protection. Inactivation of skn-1 genetically or by RNAi strongly blocked the protective effects of coffee extract, indicating that activation of the skn-1 pathway was the primary mechanism of coffee protection. Coffee also protected against toxicity resulting from an aggregating form of green fluorescent protein (GFP) in a skn-1-dependent manner. These results suggest that the reported protective effects of coffee in multiple neurodegenerative diseases may result from a general activation of the Nrf2 phase II detoxification pathway.

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“…This may be responsible for the generation of ROS following UVA radiation, which may mediate Nrf2 activation and its accumulation in the nucleus (36). Previous studies have demonstrated that increased Nrf2 mRNA expression occurs due to UVA-induced oxidative stress (37,38). Additionally, Marrot et al (39) elucidated that UVA radiation promotes the expression of phase2 enzymes, particularly heme oxygenase 1, in keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

The effects of phototherapy and melanocytes on keratinocytes

Tang

et al. 2018

Exp Ther Med

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Abstract. Phototherapy is widely used in the treatment of vitiligo. Previous studies have focused on the effects of ultraviolet (UV) radiation on melanocytes; however, the biological effects of phototherapy and melanocytes on keratinocytes remain to be elucidated. To investigate and assess the effects of clinically doses of broad band (BB)-UVA, narrow band (NB)-UVB and melanocytes on human keratinocytes in vitro, clinical doses of BB-UVA or NB-UVB radiation and human melanoma cell A375 co-culture were performed as stress divisors to HaCaT cells. Cell proliferation, expression of protease-activated receptor-2 (PAR-2) and nuclear factor E2-related factor 2 mRNA, lipid peroxidation and intracellular antioxidant level of keratinocytes were analyzed. It was demonstrated that UV radiation inhibited the proliferation of cells apart from following exposure to low dose (1 J/cm 2 ) UVA. Medium dose (5 J/cm 2 ) UVA radiation had no adverse effects on lipid peroxidation and increased antioxidant levels in HaCaT cells. Medium (200 mJ/cm 2 ) and high (400 mJ/cm 2 ) doses of UVB radiation induced cellular damage due to increased lipid peroxidation as indicated by levels of malondialdehyde. Furthermore, A375 co-culture treatment induced a similar effect on the lipid peroxidation of HaCaT as with low dose UVB radiation. Therefore, the results of the present study determined that clinical doses of BB-UVA and NB-UVB radiation had varying effects on proliferation and related protein levels in HaCaT cells. Co-culture with A375 had similar effects as those of low dose UVA and UVB radiation, in which the PAR-2 expression was significantly upregulated.

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Essential role of Nrf2 in keratinocyte protection from UVA by quercetin

Cited by 78 publications

References 31 publications

Nrf2-mediated protection against UVA radiation in human skin keratinocytes

Nrf2-mediated protection against UVA radiation in human skin keratinocytes

Genetic Mechanisms of Coffee Extract Protection in aCaenorhabditis elegansModel of β-Amyloid Peptide Toxicity

The effects of phototherapy and melanocytes on keratinocytes

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