Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-2-26
pubmed:abstractText
S100A2 is a homodimeric protein that undergoes oxidative cross-linking and translocation from the nucleus to the cytosol in the context of oxidative stress. Suggestive of a role for S100A2 in the cutaneous response to ultraviolet light, we found altered S100A2 immunostaining in photodamaged human skin, and crosslinking of S100A2 after ultraviolet A (UVA) irradiation of normal human keratinocytes (NHK). Skin from mice, rats, and rabbits did not contain S100A2 protein, whereas skin samples from pigs, frogs and humans were strongly positive. Survival after UVA irradiation was significantly greater in NHK compared to mouse keratinocytes, suggesting a protective role for S100A2. To test this hypothesis in vivo, we expressed S100A2 in SKH2/J hairless mice under the control of a bovine keratin 5 promoter, and compared responses of TG and WT mice from 1 to 7 days after a single dose (0.5-1 MED) of solar-simulated radiation (SSR) from UVA-340 bulbs. WT and TG mice manifested a similarly robust response to SSR, characterized by epidermal hyperplasia, marked induction of p21(WAF), and a twofold increase in p53. Thymine dimers (TD) were markedly increased in the epidermis and the dermis, but while over 95% of the epidermal TD were removed by 5-6 days, elevated dermal TD persisted nearly unchanged for 7 days. Global transcriptional profiling of WT and TG mice revealed strong induction of multiple transcripts, including keratins K6 and K16, defensin beta 3, S100A8, S100A9, Sprr2i and Sprr2f. However, the only S100A2-dependent difference we observed was an induction of Cxcl13 transcripts in TG, but not WT mice (4.4-fold vs. 0.7-fold, n = 3, P = 0.022). This finding was confirmed in an independent set of mice analyzed by quantitative RT-PCR (8.8-fold vs. 1.2-fold, n = 4, P = 0.001). The finding of persistent dermal DNA damage after suberythemal doses of SSR merits further study.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1432-069X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
301
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
205-17
pubmed:meshHeading
pubmed-meshheading:18773213-Animals, pubmed-meshheading:18773213-Cells, Cultured, pubmed-meshheading:18773213-Chemokine CXCL13, pubmed-meshheading:18773213-Chemotactic Factors, pubmed-meshheading:18773213-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:18773213-Dose-Response Relationship, Radiation, pubmed-meshheading:18773213-Gene Expression Regulation, pubmed-meshheading:18773213-Humans, pubmed-meshheading:18773213-Keratinocytes, pubmed-meshheading:18773213-Mice, pubmed-meshheading:18773213-Mice, Hairless, pubmed-meshheading:18773213-Mice, Transgenic, pubmed-meshheading:18773213-Models, Animal, pubmed-meshheading:18773213-Psoriasis, pubmed-meshheading:18773213-RNA, Messenger, pubmed-meshheading:18773213-S100 Proteins, pubmed-meshheading:18773213-Skin, pubmed-meshheading:18773213-Transplantation, Heterologous, pubmed-meshheading:18773213-Tumor Suppressor Protein p53, pubmed-meshheading:18773213-Ultraviolet Rays
pubmed:year
2009
pubmed:articleTitle
Transgenic expression of S100A2 in hairless mouse skin enhances Cxcl13 mRNA in response to solar-simulated radiation.
pubmed:affiliation
Department of Dermatology, University of Michigan, Ann Arbor, MI 48109-0932, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't