Upregulation of Cell-Surface-Associated Plasminogen Activation in Cultured Keratinocytes by Interleukin-1βand Tumor Necrosis Factor-α

Bechtel, Michael; Reinartz, Jeannette; Rox, Jutta M.; Inndorf, Stefan; Schaefer, Birgit M.; Kramer, Michael D.

doi:10.1006/excr.1996.0094

Cited by 49 publications

(28 citation statements)

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“…The mechanisms of IL-1 signaling involved in susceptibility to respiratory diseases are unknown. However, IL-1 signaling can induce the expression of the activators of ECM degradation [51], [52], [53]. Therefore, we hypothesize that high expression of IL-1 agonists and high ECM turnover render tissues susceptible to viral infections and vesicular lesions.…”

Section: Discussionmentioning

confidence: 98%

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

et al. 2013

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Foot-and-mouth disease virus (FMDV) targets specific tissues for primary infection, secondary high-titer replication (e.g. foot and mouth where it causes typical vesicular lesions) and long-term persistence at some primary replication sites. Although integrin αVβ6 receptor has been identified as primary FMDV receptors in animals, their tissue distribution alone fails to explain these highly selective tropism-driven events. Thus, other molecular mechanisms must play roles in determining this tissue specificity. We hypothesized that differences in certain biological activities due to differential gene expression determine FMDV tropism and applied whole genome gene expression profiling to identify genes differentially expressed between FMDV-targeted and non-targeted tissues in terms of supporting primary infection, secondary replication including vesicular lesions, and persistence. Using statistical and bioinformatic tools to analyze the differential gene expression, we identified mechanisms that could explain FMDV tissue tropism based on its association with differential expression of integrin αVβ6 heterodimeric receptor (FMDV receptor), fibronectin (ligand of the receptor), IL-1 cytokines, death receptors and the ligands, and multiple genes in the biological pathways involved in extracellular matrix turnover and interferon signaling found in this study. Our results together with reported findings indicate that differences in (1) FMDV receptor availability and accessibility, (2) type I interferon-inducible immune response, and (3) ability to clear virus infected cells via death receptor signaling play roles in determining FMDV tissue tropism and the additional increase of high extracellular matrix turnover induced by FMDV infection, likely via triggering the signaling of highly expressed IL-1 cytokines, play a key role in the pathogenesis of vesicular lesions.

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Section: Discussionmentioning

confidence: 98%

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

et al. 2013

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“…These findings suggest that the expression of both the ligand and its receptor may be regulated by the same factors. Evidence for this co-ordinated regulation of uPA and uPAR was recently obtained using cultured keratinocytes (Bechtel et al, 1996). Using these cells, levels of both uPA and its receptor were induced by interleukin-13 and tumour necrosis factor-a.…”

Section: Immunostaining For Uparmentioning

confidence: 91%

Semi-quantitation of urokinase plasminogen activator and its receptor in breast carcinomas by immunocytochemistry

Kennedy

Duffy²,

Duggan³

et al. 1998

Br J Cancer

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Summary Urokinase plasminogen activator (uPA) is a serine protease involved in cancer invasion and metastasis. uPA acts in vivo by binding to a membrane receptor known as uPAR. In this study, uPA and uPAR levels were semiquantitated by immunocytochemistry in 36 primary breast carcinomas. Using monoclonal antibody HD-UK 1, uPA was detected both in stromal and in malignant cells. However, the predominant location was in the stromal cells. Using double-staining, cells containing uPA were also found to coexpress either cytokeratin (an epithelial cell marker) or more frequently KP1 (a macrophage/monocyte cell marker). With monoclonal antibody HD-uPAR 13.1, uPAR was localized principally to spindle-or macrophage-like stromal cells, especially when these cells surrounded invasive breast cancer. In contrast, uPAR was only rarely detected in cancer cells and was not detected in normal epithelia surrounding tumour or in areas of adenosis. uPA levels in both stromal and epithelial cells were significantly correlated with those for uPAR. We conclude that both uPA and its receptor are mostly present in stromal cells in invasive breast carcinomas. These results suggest that stromal cells collaborate with malignant cells to mediate metastasis.

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“…secreted for example by keratinocytes. elicits a protease cascade leading to activated plasmin (Bechtel et al 1996). It was reported that uPA colocalizes pericellularly with the QvP5 vitronectin receptor subty-pe.…”

Section: Autocrine Stimulation Of C-mycmentioning

confidence: 99%

“…TNF-a also induces plasminogen actixator/urokinase (uPA) by the NTFKB pathwav (Meichle et al 1990: Noxak et al 1991. This protease might sen-e a phy siological role upon TNT-a induction in xxound healing and tissue remodelling (Bechtel et al 1996). and also a pathological role during malignant progression (Delbaldo et al 1995).…”

mentioning

confidence: 99%

Autocrine self-elimination of cultured ovarian cancer cells by tumour necrosis factor α (TNF-α)

Simonitsch

Krupitza²

1998

Br J Cancer

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Human ovarian adenocarcinoma cells N.1 secrete an autocrine activity that stimulates active cell death under serum-reduced conditions. To substitute the autocrine activity by a single physiological component, 28 cytokines, growth factors and biomodulators were tested [interleukin 1alpha (IL-1alpha), IL-1beta, IL-2, IL-3, IL-4, IL-6, IL-10, IL-11, stem cell factor (SCF), platelet-derived growth factor (PDGF), acid fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF-1), IGF-2, insulin, macrophage colony-stimulating factor (M-CSF), granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), oncostatin, RANTES (regulated on activation normal T cell expressed and secreted), angiogenin, leukaemia inhibitory factor (LIF), erythropoietin (EPO), interferon alpha (INF-alpha), INF-gamma, transferrin, tumour necrosis factor alpha (TNF-alpha, TNF-beta and bovine serum albumin for control reasons]. In these experiments, only TNF-alpha and TNF-beta rapidly induced apoptosis. TNF-alpha and TNF-receptor 1 were expressed by N.1 cells, and the secretion of TNF-alpha was verified by enzyme-linked immunosorbent assay (ELISA). Autocrine factor-triggered apoptosis was inhibited when conditioned supernatant was preincubated with anti-TNF-alpha antibody. These findings suggested that the apoptosis-inducing component of the N.1 autocrine activity was TNF-alpha. In the presence of antisense c-myc oligonucleotides, induction of cell death by autocrine factor was partly inhibited. Autocrine factor and TNF-alpha stimulated transcription of the invasiveness-related protease plasminogen activator/urokinase mRNA (upa) with similar kinetics. When N.1 cells were exposed to purified plasminogen activator/urokinase protein (uPA), cell matrix contact was disrupted. Thus, uPA might serve a physiological role during TNF-induced apoptosis by affecting the interactions between cells and the basal membrane, thereby facilitating anoikis. This mechanistic study, which was restricted to a single human ovarian carcinoma model cell line (N.1), provides evidence that N.1 maintains the capacity to undergo c-myc-dependent apoptosis by the TNF-TNF-receptor pathway, and no additional pharmacological stimuli for induction of apoptosis are required. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 6 Figure 8

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Upregulation of Cell-Surface-Associated Plasminogen Activation in Cultured Keratinocytes by Interleukin-1βand Tumor Necrosis Factor-α

Cited by 49 publications

References 0 publications

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

Semi-quantitation of urokinase plasminogen activator and its receptor in breast carcinomas by immunocytochemistry

Autocrine self-elimination of cultured ovarian cancer cells by tumour necrosis factor α (TNF-α)

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