Regulation of Tristetraprolin Expression by Interleukin-1β and Dexamethasone in Human Pulmonary Epithelial Cells: Roles for Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase

@article{King2009RegulationOT,
  title={Regulation of Tristetraprolin Expression by Interleukin-1$\beta$ and Dexamethasone in Human Pulmonary Epithelial Cells: Roles for Nuclear Factor-$\kappa$B and p38 Mitogen-Activated Protein Kinase},
  author={Elizabeth M. King and Manminder Kaur and Wei Gong and Christopher F. Rider and Neil S Holden and Robert Newton},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2009},
  volume={330},
  pages={575 - 585}
}
The mRNA-destabilizing protein tristetraprolin (TTP) negatively regulates adenine- and uridine-rich element (ARE)-containing mRNAs. In A549 pulmonary cells, TTP mRNA and both a ∼40- and a ∼45-kDa phosphorylated version of TTP protein were rapidly induced in response to interleukin (IL)-1β. Analysis with IκBαΔN, a dominant version of inhibitor of κBα (IκBα), as well as dominant-negative and small-molecule IκB kinase (IKK) inhibitors demonstrated that IL-1β-induced TTP is nuclear factor-κB (NF-κB… 
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MK2 posttranscriptionally regulates TNF-α-induced expression of ICAM-1 and IL-8 via tristetraprolin in human pulmonary microvascular endothelial cells.
TLDR
Results suggest that MK2, in HPMECs, regulates TNF-α-induced expression of ICAM-1 and IL-8 via TTP at the mRNA decay level.
Mitogen-Activated Protein Kinase Phosphatase-1 Negatively Regulates the Expression of Interleukin-6, Interleukin-8, and Cyclooxygenase-2 in A549 Human Lung Epithelial Cells
TLDR
Inflammatory-induced MKP-1 expression was found to negatively regulate p38 phosphorylation and the expression of IL-6, IL-8, and COX-2 in human pulmonary epithelial cells, and compounds that enhance MKp-1 may have anti-inflammatory effects and control inflammatory response in the human lung.
Activating protein phosphatase 2A (PP2A) enhances tristetraprolin (TTP) anti-inflammatory function in A549 lung epithelial cells.
Transcriptional regulation of tristetraprolin by NF-κB signaling in LPS-stimulated macrophages
TLDR
Physical interaction analysis including oligonucleotides competition, gel shift and chromatin immunoprecipitation assays demonstrated that NF-κB activated by LPS or TNFα bound to the TTP promoter specifically, suggesting that during LPS stimulation, NF-kkB signaling were activated to regulate the transcription of TTP mRNA.
Roles for the Mitogen-activated Protein Kinase (MAPK) Phosphatase, DUSP1, in Feedback Control of Inflammatory Gene Expression and Repression by Dexamethasone*
TLDR
Despite general roles in feedback inhibition, DUSP1 plays a transient, often partial, role in the dexamethasone-dependent repression of certain inflammatory genes, illustrating key roles for D USP1-independent effectors in mediating glucocorticoid- dependent repression.
EGF activates TTP expression by activation of ELK-1 and EGR-1 transcription factors
TLDR
The results demonstrate the induction of the gene coding TTP (ZFP36) by EGF through the ERK1/2-dependent pathway and implicates the transcription factor ELK-1 in this process, which regulates ZFP36 expression by two mechanisms: by binding the Z FP36 promoter directly through ETS-binding site and by inducing expression of EGR-1.
Negative Feed-forward Control of Tumor Necrosis Factor (TNF) by Tristetraprolin (ZFP36) Is Limited by the Mitogen-activated Protein Kinase Phosphatase, Dual-specificity Phosphatase 1 (DUSP1)
TLDR
A regulatory network, whereby DUSP1-dependent negative feedback control reduces feed-forward control by ZFP36-dependent and -independent mechanisms is confirmed, whereby MAPK inhibition initially attenuates TNF mRNA, but reduced feed- forward control subsequently produces an increase.
Transcriptional regulation of the anti-inflammatory protein tristetraprolin (TTP)
TLDR
Three putative regulatory elements located upstream of the \(Zfp36\) locus were shown to mediate cooperative transcriptional regulation by various combinations of pro- and anti-inflammatory agonists.
Tristetraprolin-dependent Post-transcriptional Regulation of Inflammatory Cytokine mRNA Expression by Apolipoprotein A-I
TLDR
This study has for the first time found that apoA-I suppresses the expression of some inflammatory cytokines induced by lipopolysaccharide via a specific post-transcriptional regulation process, namely mRNA destabilization, in macrophages.
The RNA-binding protein Tristetraprolin (TTP) is a critical negative regulator of the NLRP3 inflammasome
TLDR
It is found that human NLRP3 can be alternatively polyadenylated, producing a short 3′-UTR isoform that excludes regulatory elements, including the TTP- and miRNA-223-binding sites.
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