Activation of the Human RANTES Gene Promoter in a Macrophage Cell Line by Lipopolysaccharide Is Dependent on Stress-Activated Protein Kinases and the IκB Kinase Cascade: Implications for Exacerbation of Allergic Inflammation by Environmental Pollutants

Hiura, Timothy S.; Kempiak, Stephan J.; Nel, André E.

doi:10.1006/clim.1998.4659

Cited by 40 publications

(28 citation statements)

References 38 publications

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“…We also found Syk expression in human nasal polyp-derived fibroblasts. LPS augments tyrosine phosphorylation (11,12,14), which results in phosphorylation or activation of mitogen-activated protein (MAP) kinases: 44-and 42-kDa MAP kinases (extracellular signal-related kinase 1 and 2) (14, 32), stress-activated protein kinase/ JNK (33), and p38 kinase (10,14,34). In this study, we demonstrated that LPS induced tyrosine phosphorylation of Syk and activated JNK1 in nasal fibroblast lines.…”

Section: Discussionmentioning

confidence: 76%

“…Tyrosine phosphorylation of MAP kinase is associated with LPS-induced TNF-␣ production in mice (13). RANTES mRNA expressions were induced through the activation of MAP kinases in endothelial cells (32), or through JNK and NF-B kinase cascades in macrophages stimulated with LPS (33). The Syk-generated signal cooperates to enhance Racinduced JNK activation in T lymphocytes (35), and MAP kinase activation was compromised in the macrophages of Syk Ϫ/Ϫ mice after Fc-␥ receptor stimulation (36).…”

Section: Discussionmentioning

confidence: 99%

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Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

Yamada

Fujieda

Yanagi

et al. 2001

The Journal of Immunology

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Fibroblasts, a rich source of chemokines, interact with eosinophils and play a key role in the pathogenesis of airway disease. RANTES is produced by fibroblasts to attract and activate eosinophils. LPS is known to induce RANTES and cause protein tyrosine phosphorylation. Nonreceptor protein tyrosine kinase Syk is widely expressed and an important role in intracellular signal transduction in hemopoietic cells. In the present study, we examined whether Syk was expressed in a number of primary human nasal polyp tissue-derived fibroblast lines and whether it played some role in cellular function. Syk proteins were expressed in human nasal fibroblasts, but the expression level varied. There were positive correlations between the level of Syk expression and RANTES production induced by LPS. Overexpression of wild-type Syk by gene transfer enhanced RANTES production from nasal fibroblasts stimulated with LPS. The decrease of Syk expression by the administration of Syk antisense inhibited RANTES production. These results suggest that Syk expression affects RANTES production in fibroblasts of nasal polyps.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

Yamada

Fujieda

Yanagi

et al. 2001

The Journal of Immunology

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“…[45][46][47][48][49][50] IL-1 and TNF induced CCL3 and CCL4 production by several hepatoma cell lines and an immunohistochemical analysis demonstrated the presence of IL-1␣ and IL-1␤ in hepatoma tissues. Thus, it is reasonable to speculate that endogenously produced IL-1 induces CCL3 production in an autocrine and/or paracrine manner.…”

Section: Discussionmentioning

confidence: 95%

Potential Interaction between CCR1 and Its Ligand, CCL3, Induced by Endogenously Produced Interleukin-1 in Human Hepatomas

Nakamoto

Nemoto-Sasaki

et al. 2003

The American Journal of Pathology

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Hepatoma cell lines can produce a massive amount of chemokines in response to various stimuli including hepatitis viruses and their products. However, it remains elusive on the types of chemokine receptor(s) expressed in the hepatoma tissues and its roles in hepatoma development. To clarify these points, we examined the chemokine receptor expression in six human hepatoma cell lines. All of the hepatoma cell lines constitutively and exclusively expressed CCR1 mRNA and its protein on their cell surface. CCR1 expression was also detected on hepatoma cells and to a lesser degree, on endothelial cells in hepatoma tissues but not in normal liver tissues. Furthermore, CCL3 expression was detected in hepatoma cells, endothelial cells, and to a lesser degree, fibroblast-like cells in hepatoma tissue, whereas only occasional vascular endothelial cells and inflammatory cells in normal liver tissues were weakly positive for CCL3. Moreover, the forskolin-mediated increases in intracellular cAMP concentrations were inhibited by the ligands for CCR1, CCL3, CCL4, and CCL5, suggesting that the expressed CCR1 was functional.

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“…In contrast, much less is known about the regulation of RANTES mRNA in MTECs. In LPS-stimulated macrophage cell line, RAW264.7 cells, it was shown that JNK and NF-B response elements were involved in RANTES gene activation (47). Besides, both p38 MAPK and JNK signaling pathways regulate RANTES production in influenza virus-infected human bronchial epithelial cells (48).…”

Section: Discussionmentioning

confidence: 99%

Roles of Toll-Like Receptors in C-C Chemokine Production by Renal Tubular Epithelial Cells

Tsuboi¹,

Yoshikai

Matsuo³

et al. 2002

The Journal of Immunology

219

198

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Pyelonephritis, in which renal tubular epithelial cells are directly exposed to bacterial component, is a major predisposing cause of renal insufficiency. Although previous studies have suggested C-C chemokines are involved in the pathogenesis, the exact source and mechanisms of the chemokine secretion remain ambiguous. In this study, we evaluated the involvement of Toll-like receptors (TLRs) in C-C chemokine production by mouse primary renal tubular epithelial cells (MTECs). MTECs constitutively expressed mRNA for TLR1, 2, 3, 4, and 6, but not for TLR5 or 9. MTECs also expressed MD-2, CD14, myeloid differentiation factor 88, and Toll receptor-IL-1R domain-containing adapter protein/myeloid differentiation factor 88-adapter-like. Synthetic lipid A and lipoprotein induced monocyte chemoattractant protein 1 (MCP-1) and RANTES production in MTECs, which strictly depend on TLR4 and TLR2, respectively. In contrast, MTECs were refractory to CpG-oligodeoxynucleotide in chemokine production, consistently with the absence of TLR9. LPS-mediated MCP-1 and RANTES production in MTECs was abolished by NF-κB inhibition, but unaffected by extracellular signal-regulated kinase inhibition. In LPS-stimulated MTECs, inhibition of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase significantly decreased RANTES, but did not affect MCP-1 mRNA induction. Thus, MTECs have a distinct expression pattern of TLR and secrete C-C chemokines in response to direct stimulation with a set of bacterial components.

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Activation of the Human RANTES Gene Promoter in a Macrophage Cell Line by Lipopolysaccharide Is Dependent on Stress-Activated Protein Kinases and the IκB Kinase Cascade: Implications for Exacerbation of Allergic Inflammation by Environmental Pollutants

Cited by 40 publications

References 38 publications

Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

Protein-Tyrosine Kinase Syk Expressed in Human Nasal Fibroblasts and Its Effect on RANTES Production

Potential Interaction between CCR1 and Its Ligand, CCL3, Induced by Endogenously Produced Interleukin-1 in Human Hepatomas

Roles of Toll-Like Receptors in C-C Chemokine Production by Renal Tubular Epithelial Cells

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