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| pubmed-article:19874887 | lifeskim:mentions | umls-concept:C1415620 | lld:lifeskim |
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| pubmed-article:19874887 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:19874887 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:19874887 | pubmed:dateCreated | 2010-2-3 | lld:pubmed |
| pubmed-article:19874887 | pubmed:abstractText | Ultraviolet A (UVA) radiation is an oxidizing agent that strongly induces the heme oxygenase 1 (HO-1) gene and expression of the protein in cultured human skin fibroblasts but weakly induces it in skin keratinocytes. Lower basal levels of HO-1 and much higher basal levels of HO-2 protein are observed in keratinocytes compared with fibroblasts. Using both overexpression and knockdown approaches, we demonstrate that HO-2 modulates basal and UVA-induced HO-1 protein levels, whereas HO-1 levels do not affect HO-2 levels in skin fibroblasts and keratinocytes. Silencing of Bach1 strongly increases HO-1 levels in transformed HaCaT keratinocytes and these HO-1 levels are not further increased by either UVA irradiation or silencing of HO-2. This is consistent with the conclusion that high constitutive levels of HO-2 expression in keratinocytes are responsible for the resistance of these cells to HO-1 induction by UVA radiation and that Bach1 plays a predominant role in influencing the lack of HO-1 expression in keratinocytes. Bach1 inhibition leading to HO-1 induction reduced UVA-irradiation-induced damage as monitored both by the extent of LDH release and by nuclear condensation, so that Bach1 inhibition seems to protect against UVA-irradiation-induced damage in keratinocytes. | lld:pubmed |
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| pubmed-article:19874887 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19874887 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19874887 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19874887 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19874887 | pubmed:issn | 1873-4596 | lld:pubmed |
| pubmed-article:19874887 | pubmed:author | pubmed-author:TyrrellRex... | lld:pubmed |
| pubmed-article:19874887 | pubmed:author | pubmed-author:ZhongJulia... | lld:pubmed |
| pubmed-article:19874887 | pubmed:author | pubmed-author:EdwardsGavin... | lld:pubmed |
| pubmed-article:19874887 | pubmed:author | pubmed-author:RavalChintanC | lld:pubmed |
| pubmed-article:19874887 | pubmed:copyrightInfo | Copyright 2009 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:19874887 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19874887 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19874887 | pubmed:volume | 48 | lld:pubmed |
| pubmed-article:19874887 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19874887 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19874887 | pubmed:pagination | 196-206 | lld:pubmed |
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| pubmed-article:19874887 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:19874887 | pubmed:articleTitle | A role for Bach1 and HO-2 in suppression of basal and UVA-induced HO-1 expression in human keratinocytes. | lld:pubmed |
| pubmed-article:19874887 | pubmed:affiliation | Department of Pharmacy and Pharmacology, University of Bath, Bath BA2 7AY, UK. | lld:pubmed |
| pubmed-article:19874887 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19874887 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:19874887 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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