Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2005-5-18
pubmed:abstractText
UV radiation is an important etiologic factor for skin cancer, including melanoma. Constitutive pigmentation and the ability to tan are considered the main photoprotective mechanism against sun-induced carcinogenesis. Pigmentation in the skin is conferred by epidermal melanocytes that synthesize and transfer melanin to keratinocytes. Therefore, insuring the survival and genomic stability of epidermal melanocytes is critical for inhibiting photocarcinogenesis, particularly melanoma, the most deadly form of skin cancer. The paracrine factors alpha-melanocortin and endothelin-1 are critical for the melanogenic response of cultured human melanocytes to UV radiation. We report that alpha-melanocortin and endothelin-1 rescued human melanocytes from UV radiation-induced apoptosis and reduced DNA photoproducts and oxidative stress. The survival effects of alpha-melanocortin and endothelin-1 were mediated by activation of the melanocortin 1 and endothelin receptors, respectively. Treatment of melanocytes with alpha-melanocortin and/or endothelin-1 before exposure to UV radiation activated the inositol triphosphate kinase-Akt pathway and increased the phosphorylation and expression of the microphthalmia-related transcription factor. Treatment with alpha-melanocortin and/or endothelin-1 enhanced the repair of cyclobutane pyrimidine dimers and reduced the levels of hydrogen peroxide induced by UV radiation. These effects are expected to reduce genomic instability and mutagenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/AKT1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1, http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide, http://linkedlifedata.com/resource/pubmed/chemical/MITF protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Microphthalmia-Associated..., http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/alpha-MSH
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4292-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15899821-Adult, pubmed-meshheading:15899821-Apoptosis, pubmed-meshheading:15899821-DNA, pubmed-meshheading:15899821-DNA Damage, pubmed-meshheading:15899821-DNA-Binding Proteins, pubmed-meshheading:15899821-Endothelin-1, pubmed-meshheading:15899821-Enzyme Activation, pubmed-meshheading:15899821-Humans, pubmed-meshheading:15899821-Hydrogen Peroxide, pubmed-meshheading:15899821-Melanocytes, pubmed-meshheading:15899821-Microphthalmia-Associated Transcription Factor, pubmed-meshheading:15899821-Protein-Serine-Threonine Kinases, pubmed-meshheading:15899821-Proto-Oncogene Proteins, pubmed-meshheading:15899821-Proto-Oncogene Proteins c-akt, pubmed-meshheading:15899821-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:15899821-Transcription Factors, pubmed-meshheading:15899821-Ultraviolet Rays, pubmed-meshheading:15899821-alpha-MSH
pubmed:year
2005
pubmed:articleTitle
alpha-Melanocortin and endothelin-1 activate antiapoptotic pathways and reduce DNA damage in human melanocytes.
pubmed:affiliation
Department of Dermatology, University of Cincinnati College of Medicine and Shriners' Burns Institute, Cincinnati, Ohio 45267-0592, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural