pubmed-article:12884291 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C0032636 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C0024880 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C1332102 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C1428495 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C1819459 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:12884291 | lifeskim:mentions | umls-concept:C0279078 | lld:lifeskim |
pubmed-article:12884291 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:12884291 | pubmed:dateCreated | 2003-7-28 | lld:pubmed |
pubmed-article:12884291 | pubmed:abstractText | Mast cells are exposed to an oxidative environment in the course of allergic and inflammatory reactions. We have examined the effects of H(2)O(2) stimulation in a primary rat basophilic leukemia cell line (RBL-2H3) and compared with IgE-dependent stimulation. Like IgE stimulation, H(2)O(2) up-regulates IL-4 and IL-6 gene expression and cytokine secretion, shows a little effect on IL-5 but does not induce IL-10 gene expression. Simultaneous H(2)O(2) treatment and FcepsilonRI triggering of mast cells has additive effects on IL-4 expression. In addition, we show that both stimuli induce the nuclear translocation of APE/Ref-1, a bifunctional enzyme that stimulates the DNA-binding activity of several transcription factors through the reduction of highly reactive cysteines. Conditional inactivation of APE/Ref-1 expression abolishes H(2)O(2)-induced IL-4 and IL-6 gene expression but does not affect that induced by FcepsilonRI stimulation. Our findings indicate that oxidative stress activates the gene expression of a specific cytokine pattern in mast cells through an APE/Ref-1-dependent pathway, which is distinct from the one that is activated by FcepsilonRI stimulation. Nonetheless, H(2)O(2) and FcepsilonRI signalings are additive in augmenting IL-4 production. Most importantly, oxidative stress can induce a pro-type 2 inflammatory response from mast cells that is independent of FcepsilonRI stimulation. | lld:pubmed |
pubmed-article:12884291 | pubmed:language | eng | lld:pubmed |
pubmed-article:12884291 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12884291 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12884291 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12884291 | pubmed:month | Aug | lld:pubmed |
pubmed-article:12884291 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:12884291 | pubmed:author | pubmed-author:RiveraJuanJ | lld:pubmed |
pubmed-article:12884291 | pubmed:author | pubmed-author:PucilloCarloC | lld:pubmed |
pubmed-article:12884291 | pubmed:author | pubmed-author:FrossiBarbara... | lld:pubmed |
pubmed-article:12884291 | pubmed:author | pubmed-author:De... | lld:pubmed |
pubmed-article:12884291 | pubmed:author | pubmed-author:DanielKenn... | lld:pubmed |
pubmed-article:12884291 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12884291 | pubmed:volume | 33 | lld:pubmed |
pubmed-article:12884291 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12884291 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12884291 | pubmed:pagination | 2168-77 | lld:pubmed |
pubmed-article:12884291 | pubmed:dateRevised | 2011-8-4 | lld:pubmed |
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pubmed-article:12884291 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12884291 | pubmed:articleTitle | Oxidative stress stimulates IL-4 and IL-6 production in mast cells by an APE/Ref-1-dependent pathway. | lld:pubmed |
pubmed-article:12884291 | pubmed:affiliation | Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Udine, Udine, Italy. | lld:pubmed |
pubmed-article:12884291 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12884291 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:79116 | entrezgene:pubmed | pubmed-article:12884291 | lld:entrezgene |
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