Source:http://linkedlifedata.com/resource/pubmed/id/19474803
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2009-10-14
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| pubmed:abstractText |
Previous studies have found that signaling by the estrogen receptor-beta (Er-beta) attenuated solar-simulated UV radiation (SSUV)-induced immunosuppression. This study seeks evidence for a common mechanism for this immunoprotection for both Er-beta signaling and irradiation with the UVA waveband. In Skh:hr-1 hairless mice, the immunoprotection afforded by UVA exposure against subsequent UVB or cis-urocanic acid suppression of contact hypersensitivity (CHS) was abrogated by treatment with the antiestrogen, ICI 182,780. Furthermore, in normal C57BL mice, UVA enrichment of UVA/UVB sources provided protection against UVB-suppressed CHS and upregulated epidermal IL-10 expression, but this protection was inhibited in Er-beta-/- mice. These observations indicated that the immunoprotective response to UVA was dependent on Er-beta signaling. As earlier studies have established that UVA photoimmune protection depends on the induction of the stress enzyme, heme oxygenase (HO)-1, its activity was examined relative to Er-beta. Immunoprotection against SSUV by 17-beta-estradiol was prevented by inhibiting HO enzyme activity; immunoprotection against cis-urocanic acid by carbon monoxide (HO product) was prevented by ICI 182,780. In addition, the HO-1 gene was unresponsive to UVA induction in Er-beta-/- mice. Therefore, HO-1 inducibility and Er-beta signaling are interdependent requisite responses to the UVA waveband for its immunoprotective action against UVB exposure.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogen Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogen Receptor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Metalloporphyrins,
http://linkedlifedata.com/resource/pubmed/chemical/Protoporphyrins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Urocanic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/fulvestrant,
http://linkedlifedata.com/resource/pubmed/chemical/tin protoporphyrin IX
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1523-1747
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
129
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2702-10
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| pubmed:meshHeading |
pubmed-meshheading:19474803-Animals,
pubmed-meshheading:19474803-Enzyme Inhibitors,
pubmed-meshheading:19474803-Epidermis,
pubmed-meshheading:19474803-Estradiol,
pubmed-meshheading:19474803-Estrogen Antagonists,
pubmed-meshheading:19474803-Estrogen Receptor beta,
pubmed-meshheading:19474803-Female,
pubmed-meshheading:19474803-Heme Oxygenase-1,
pubmed-meshheading:19474803-Immune Tolerance,
pubmed-meshheading:19474803-Interleukin-10,
pubmed-meshheading:19474803-Metalloporphyrins,
pubmed-meshheading:19474803-Mice,
pubmed-meshheading:19474803-Mice, Hairless,
pubmed-meshheading:19474803-Mice, Inbred C57BL,
pubmed-meshheading:19474803-Mice, Mutant Strains,
pubmed-meshheading:19474803-Protoporphyrins,
pubmed-meshheading:19474803-RNA, Messenger,
pubmed-meshheading:19474803-Signal Transduction,
pubmed-meshheading:19474803-Ultraviolet Rays,
pubmed-meshheading:19474803-Urocanic Acid
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| pubmed:year |
2009
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| pubmed:articleTitle |
Interdependence between heme oxygenase-1 induction and estrogen-receptor-beta signaling mediates photoimmune protection by UVA radiation in mice.
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| pubmed:affiliation |
Faculty of Veterinary Science, University of Sydney, New South Wales, Australia. vreeve@usyd.edu.au
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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