Interleukin-1β and Tumor Necrosis Factor-α Induce MUC5AC Overexpression through a Mechanism Involving ERK/p38 Mitogen-activated Protein Kinases-MSK1-CREB Activation in Human Airway Epithelial Cells*

@article{Song2003Interleukin1AT,
  title={Interleukin-1$\beta$ and Tumor Necrosis Factor-$\alpha$ Induce MUC5AC Overexpression through a Mechanism Involving ERK/p38 Mitogen-activated Protein Kinases-MSK1-CREB Activation in Human Airway Epithelial Cells*},
  author={K. Song and W. Lee and K. Chung and J. Koo and Eun Jin Yang and J. Choi and Joo-Heon Yoon},
  journal={Journal of Biological Chemistry},
  year={2003},
  volume={278},
  pages={23243 - 23250}
}
Mucin hypersecretion is commonly observed in many inflammatory diseases of the respiratory tract. MUC5AC is generally recognized to be a major airway mucin because MUC5AC is highly expressed in the goblet cells of human airway epithelium. Moreover, it is regulated by various inflammatory cytokines. However, the mechanisms by which the interleukin (IL)-1β and tumor necrosis factor (TNF)-α induce MUC5AC gene expression in normal nasal epithelial cells, and the signal molecules involved… Expand

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References

SHOWING 1-10 OF 50 REFERENCES
Induction of MUC2 and MUC5AC Mucins by Factors of the Epidermal Growth Factor (EGF) Family Is Mediated by EGF Receptor/Ras/Raf/Extracellular Signal-regulated Kinase Cascade and Sp1*
TLDR
MUC2 and MUC5AC are two target genes of EGFR ligands in lung cancer cells, and up-regulation of these two genes goes through concomitant activation of the EGFR/Ras/Raf/Extracellular Signal-regulated Kinase-signaling pathway and Sp1 binding to their promoters. Expand
Oxidative Stress Causes Mucin Synthesis Via Transactivation of Epidermal Growth Factor Receptor: Role of Neutrophils1
TLDR
It is shown that oxidative stress causes ligand-independent activation of epidermal growth factor receptors (EGFR) and subsequent activation of mitogen-activated protein kinase kinase (MEK), resulting in mucin synthesis in NCI-H292 cells, and new therapeutic approaches in airway hypersecretory diseases are provided. Expand
Requirement of Mitogen-Activated Protein Kinases and IκB Phosphorylation for Induction of Proinflammatory Cytokines Synthesis by Macrophages Indicates Functional Similarity of Receptors Triggered by Glycosylphosphatidylinositol Anchors from Parasitic Protozoa and Bacterial Lipopolysaccharide1
TLDR
The similarity of patterns of MAPK and IκB phosphorylation, the concentration of drugs required to inhibit cytokine synthesis, as well as cross-tolerization exhibited by macrophages exposed to tG PI, tGPI-mucin, or bacterial LPS suggest that receptors with the same functional properties are triggered by these different microbial glycoconjugates. Expand
T Cell Proliferation in Response to Interleukins 2 and 7 Requires p38MAP Kinase Activation*
TLDR
Inhibition of p38MAP kinase activity with a specific pyrinidyl imidazole inhibitor SB203580 that prevents activation of its downstream effector, MAPK-activating protein kinase-2, correlated with suppression of IL-2- and IL-7-driven T cell proliferation, indicating that in T cells p38 MAP kinase has a role in transducing the mitogenic signal. Expand
Interleukin-9 upregulates mucus expression in the airways.
TLDR
The studies showed that IL-9 induces expression of MUC2 and MUC5AC in human primary lung cultures and in the human muccoepidermoid NCI-H292 cell line, indicating a direct effect ofIL-9 on inducing mucin expression in these cells, and suggest that upregulation of mucin by IL- 9 might contribute to the pathogenesis of human inflammatory airway disorders, such as asthma. Expand
Role of Mitogen-Activated Protein Kinase Cascades in Mediating Lipopolysaccharide-Stimulated Induction of Cyclooxygenase-2 and IL-1β in RAW264 Macrophages1
TLDR
Two different mitogen-activated protein kinase cascades are rate limiting for the LPS-induced activation of CREB/ATF1 and the transcription of the COX-2 and IL-1β genes, suggesting that MSK1 and MSK2 may play a role in these processes and hence are potential targets for the development of novel antiinflammatory drugs. Expand
Transcriptional regulation of the 11p15 mucin genes. Towards new biological tools in human therapy, in inflammatory diseases and cancer?
TLDR
The understanding of mucin gene transcriptional regulation, which awaits more data (identification of the signaling cascades and active cis-elements within promoters and introns), will most certainly lead to the use of mucIn genes as molecular markers in cancer and molecular tools in human gene therapy, and to the synthesis of new therapeutic agents in inflammatory diseases of the epithelium. Expand
Activation of NF-kappaB via a Src-dependent Ras-MAPK-pp90rsk pathway is required for Pseudomonas aeruginosa-induced mucin overproduction in epithelial cells.
  • J. Li, W. Feng, +4 authors C. Basbaum
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1998
TLDR
It is shown that P. aeruginosa activates a c-Src-Ras-MEK1/2-MAPK-pp90rsk signaling pathway that leads to activation of nuclear factor NF-kappaB (p65/p50), which binds to a kappaB site in the 5'-flanking region of the M UC2 gene and activates MUC2 mucin transcription and opens up new therapeutic targets for cystic fibrosis. Expand
Pro-inflammatory Cytokines and Environmental Stress Cause p38 Mitogen-activated Protein Kinase Activation by Dual Phosphorylation on Tyrosine and Threonine (*)
TLDR
It is demonstrated that p38, like JNK, is activated by treatment of cells with pro-inflammatory cytokines and environmental stress and the mechanism of p38 activation is mediated by dual phosphorylation on Thr-180 and Tyr-182. Expand
IL-4 induces mucin gene expression and goblet cell metaplasia in vitro and in vivo.
TLDR
Results indicate that airway epithelial cells express IL- 4R constitutively and that IL-4 directly induces the differentiation of epithelium into mucous glycoconjugate-containing goblet cells. Expand
...
1
2
3
4
5
...