Matches in UGent Biblio for { <https://biblio.ugent.be/publication/2976305#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B282905.
- aggregation creator B282906.
- aggregation creator B282907.
- aggregation creator B282908.
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- aggregation creator person.
- aggregation date "2012".
- aggregation format "application/pdf".
- aggregation hasFormat 2976305.bibtex.
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- aggregation isPartOf urn:issn:0741-5400.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Arginase-1-independent polyamine production stimulates the expression of IL-4-induced alternatively activated macrophage markers while inhibiting LPS-induced expression of inflammatory genes".
- aggregation abstract "In macrophages, basal polyamine (putrescine, spermidine, and spermine) levels are relatively low but are increased upon IL-4 stimulation. This Th2 cytokine induces Arg1 activity, which converts arginine into ornithine, and ornithine can be decarboxylated by ODC to produce putrescine, which is further converted into spermidine and spermine. Recently, we proposed polyamines as novel agents in IL-4-dependent E-cadherin regulation in AAMs. Here, we demonstrate for the first time that several, but not all, AAM markers depend on polyamines for their IL-4-induced gene and protein expression and that polyamine dependency of genes relies on the macrophage type. Remarkably, Arg1-deficient macrophages display rather enhanced IL-4-induced polyamine production, suggesting that an Arg1-independent polyamine synthesis pathway may operate in macrophages. On the other side of the macrophage activation spectrum, LPS-induced expression of several proinflammatory genes was increased significantly in polyamine-depleted CAMs. Overall, we propose Arg1 independently produced polyamines as novel regulators of the inflammatory status of the macrophage. Indeed, whereas polyamines are needed for IL-4-induced expression of several AAM mediators, they inhibit the LPS-mediated expression of proinflammatory genes in CAMs.".
- aggregation authorList BK561779.
- aggregation endPage "699".
- aggregation issue "5".
- aggregation startPage "685".
- aggregation volume "91".
- aggregation aggregates 2976320.
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