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16169848

Source:http://linkedlifedata.com/resource/pubmed/id/16169848

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pubmed-article:16169848pubmed:abstractTextActivation of macrophages is important in chronic inflammatory disease states such as atherosclerosis. Proinflammatory cytokines such as interferon-gamma (IFN-gamma), lipopolysaccharide (LPS), or tumor necrosis factor-alpha can promote macrophage activation. Conversely, anti-inflammatory factors such as transforming growth factor-beta1 (TGF-beta1) can decrease proinflammatory activation. The molecular mediators regulating the balance of these opposing effectors remain incompletely understood. Herein, we identify Kruppel-like factor 4 (KLF4) as being markedly induced in response to IFN-gamma, LPS, or tumor necrosis factor-alpha and decreased by TGF-beta1 in macrophages. Overexpression of KLF4 in J774a macrophages induced the macrophage activation marker inducible nitric-oxide synthase and inhibited the TGF-beta1 and Smad3 target gene plasminogen activator inhibitor-1 (PAI-1). Conversely, KLF4 knockdown markedly attenuated the ability of IFN-gamma, LPS, or IFN-gamma plus LPS to induce the iNOS promoter, whereas it augmented macrophage responsiveness to TGF-beta1 and Smad3 signaling. The KLF4 induction of the iNOS promoter is mediated by two KLF DNA-binding sites at -95 and -212 bp, and mutation of these sites diminished induction by IFN-gamma and LPS. We further provide evidence that KLF4 interacts with the NF-kappaB family member p65 (RelA) to cooperatively induce the iNOS promoter. In contrast, KLF4 inhibited the TGF-beta1/Smad3 induction of the PAI-1 promoter independent of KLF4 DNA binding through a novel antagonistic competition with Smad3 for the C terminus of the coactivator p300/CBP. These findings support an important role for KLF4 as a regulator of key signaling pathways that control macrophage activation.lld:pubmed
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pubmed-article:16169848pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:16169848pubmed:articleTitleKruppel-like factor 4 is a mediator of proinflammatory signaling in macrophages.lld:pubmed
pubmed-article:16169848pubmed:affiliationProgram in Cardiovascular Transcriptional Biology, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. mfeinberg@rics.bwh.harvard.edulld:pubmed
pubmed-article:16169848pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16169848pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:16169848pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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