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- W2067022182 endingPage "2585" @default.
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- W2067022182 abstract "Abstract Ultraviolet A (UVA) radiations are responsible for deleterious effects, mainly due to reactive oxygen species (ROS) production. Alpha‐melanocyte stimulating hormone (α‐MSH) binds to melanocortin‐1 receptor (MC1R) in melanocytes to stimulate pigmentation and modulate cutaneous inflammatory responses. MC1R may be induced in keratinocytes after UV exposure. To investigate the effect of MC1R signaling on UVA‐induced ROS (UVA‐ROS) production, we generated HaCaT cells that stably express human MC1R (HaCaT‐MC1R) or the Arg151Cys (R 151 C) non‐functional variant (HaCaT‐R 151 C). We then assessed ROS production immediately after UVA exposure and found that: (1) UVA‐ROS production was strongly reduced in HaCaT‐MC1R but not in HaCaT‐R 151 C cells compared to parental HaCaT cells; (2) this inhibitory effect was further amplified by incubation of HaCaT‐MC1R cells with α‐MSH before UVA exposure; (3) protein kinase A (PKA)‐dependent NoxA1 phosphorylation was increased in HaCaT‐MC1R compared to HaCaT and HaCaT‐R 151 C cells. Inhibition of PKA in HaCaT‐MC1R cells resulted in a marked increase of ROS production after UVA irradiation; (4) the ability of HaCaT‐MC1R cells to produce UVA‐ROS was restored by inhibiting epidermal growth factor receptor (EGFR) or extracellular signal‐regulated kinases (ERK) activity before UVA exposure. Our findings suggest that constitutive activity of MC1R in keratinocytes may reduce UVA‐induced oxidative stress via EGFR and cAMP‐dependent mechanisms. J. Cell. Physiol. 227: 2578–2585, 2012. © 2011 Wiley Periodicals, Inc." @default.
- W2067022182 created "2016-06-24" @default.
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- W2067022182 date "2012-02-24" @default.
- W2067022182 modified "2023-10-10" @default.
- W2067022182 title "MC1R expression in HaCaT keratinocytes inhibits UVA-induced ROS production via NADPH Oxidase- and cAMP-dependent mechanisms" @default.
- W2067022182 cites W1488294447 @default.
- W2067022182 cites W1496980490 @default.
- W2067022182 cites W1502546829 @default.
- W2067022182 cites W1575925203 @default.
- W2067022182 cites W1752267015 @default.
- W2067022182 cites W1964628210 @default.
- W2067022182 cites W1966810184 @default.
- W2067022182 cites W1968998462 @default.
- W2067022182 cites W1969901996 @default.
- W2067022182 cites W1972985481 @default.
- W2067022182 cites W1973223056 @default.
- W2067022182 cites W1974902293 @default.
- W2067022182 cites W1976108411 @default.
- W2067022182 cites W1976552445 @default.
- W2067022182 cites W1979580952 @default.
- W2067022182 cites W1981605211 @default.
- W2067022182 cites W1984107812 @default.
- W2067022182 cites W1985248944 @default.
- W2067022182 cites W1993852996 @default.
- W2067022182 cites W1995126053 @default.
- W2067022182 cites W1995819749 @default.
- W2067022182 cites W2000253969 @default.
- W2067022182 cites W2000618536 @default.
- W2067022182 cites W2001574640 @default.
- W2067022182 cites W2001670469 @default.
- W2067022182 cites W2010014912 @default.
- W2067022182 cites W2010684135 @default.
- W2067022182 cites W2012760010 @default.
- W2067022182 cites W2012846873 @default.
- W2067022182 cites W2015877899 @default.
- W2067022182 cites W2024140056 @default.
- W2067022182 cites W2032368320 @default.
- W2067022182 cites W2034710079 @default.
- W2067022182 cites W2035040393 @default.
- W2067022182 cites W2036127346 @default.
- W2067022182 cites W2046893282 @default.
- W2067022182 cites W2051811954 @default.
- W2067022182 cites W2052167761 @default.
- W2067022182 cites W2066589243 @default.
- W2067022182 cites W2069423064 @default.
- W2067022182 cites W2070332388 @default.
- W2067022182 cites W2074179023 @default.
- W2067022182 cites W2077744618 @default.
- W2067022182 cites W2077776912 @default.
- W2067022182 cites W2080298463 @default.
- W2067022182 cites W2080578809 @default.
- W2067022182 cites W2082190322 @default.
- W2067022182 cites W2083283822 @default.
- W2067022182 cites W2083521162 @default.
- W2067022182 cites W2083630780 @default.
- W2067022182 cites W2083754582 @default.
- W2067022182 cites W2085128107 @default.
- W2067022182 cites W2088658333 @default.
- W2067022182 cites W2092984629 @default.
- W2067022182 cites W2096869450 @default.
- W2067022182 cites W2101121350 @default.
- W2067022182 cites W2102619095 @default.
- W2067022182 cites W2105515073 @default.
- W2067022182 cites W2107509703 @default.
- W2067022182 cites W2114496307 @default.
- W2067022182 cites W2115022580 @default.
- W2067022182 cites W2116893702 @default.
- W2067022182 cites W2123439746 @default.
- W2067022182 cites W2123639353 @default.
- W2067022182 cites W2131212622 @default.
- W2067022182 cites W2141577885 @default.
- W2067022182 cites W2147206627 @default.
- W2067022182 cites W2147516927 @default.
- W2067022182 cites W2153452328 @default.
- W2067022182 cites W2154229994 @default.
- W2067022182 cites W2158117735 @default.
- W2067022182 cites W2158429932 @default.
- W2067022182 cites W2159876689 @default.
- W2067022182 cites W2162141135 @default.
- W2067022182 cites W2167707357 @default.
- W2067022182 cites W2169488042 @default.
- W2067022182 cites W2169905973 @default.
- W2067022182 cites W2985120158 @default.
- W2067022182 doi "https://doi.org/10.1002/jcp.22996" @default.
- W2067022182 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21898403" @default.
- W2067022182 hasPublicationYear "2012" @default.
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