INT127691
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
CXCL1 expression is up-regulated in colorectal adenomas and adenocarcinoma [17], inhibiting apoptosis and inversely linked to expression of fibulin-1, an extra-cellular matrix protein implicated in control of tumour cell migration. | |||||||||||||||
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Wang et al. (2006) [18] reported that expression of CXCL1 induced by PGE2 was linked to angiogenesis in colorectal cancer in vitro and in vivo and thus provided a link between COX-2 up-regulation and chemokine induced tumour associated endothelial cell migration. | |||||||||||||||
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Candesartan reduced CXCL1 gene expression within the border of the ischemic lesion. | |||||||||||||||
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Gene expression of CXCL1, interleukin-6 and TNF-alpha was upregulated in ischemic brain areas of dTGR (Fig. 5). | |||||||||||||||
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Only aliskiren was able to reduce gene expression of CXCL1, interleukin-6 and TNF-alpha in the ischemic core. | |||||||||||||||
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Pre-treatment with candesartan or aliskiren attenuated this increase of CXCL1 expression 24 h post-ischemia. | |||||||||||||||
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Pretreatment with BQ-123 or BQ-788 (i.a.; 15 pmol/cavity) also decreased zymosan-induced TNF-alpha production within 6 h, keratinocyte-derived chemokine/CXCL1 production within 24 h, and leukotriene B(4) at both time-points. | |||||||||||||||
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In addition, IL-8, CXCL1, CXCL2, CXCL3, and CCL20 had higher levels of expression in the polyps compared to normal, which is in keeping with the current study. | |||||||||||||||
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Relative gene expression of CXCL1, interleukin-6 and TNF-alpha was significantly reduced in the ischemic core of dTGR treated with aliskiren (p<0.05). | |||||||||||||||
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In contrast, in the ischemic border zone there was a significant reduction of CXCL1 gene expression in animals treated with candesartan (p<0.01). | |||||||||||||||
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Arterial SMCs, in particular, express a large set of genes that mediate these interactions—such as cytokines/chemokines (IL6, CCL8, CCL7, CCL2, CXCL1, CXCL2, CXCL3, and CXCL6), complement pathway (complement factor B [CFB]), and surface receptor (ICAM1) (Figure 3B)—suggesting that vascular SMCs may themselves mediate recruitment of immune cells to the vascular walls. | |||||||||||||||
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Among CXC chemokines, IL-8/CXCL8, epithelial neutrophil-activating protein-78 (ENA-78)/CXCL5, growth-regulated oncogene-alpha (gro?) | |||||||||||||||
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Among CXC chemokines, IL-8/CXCL8, epithelial neutrophil-activating protein-78 (ENA-78)/CXCL5, growth-regulated oncogene-alpha (gro?) | |||||||||||||||
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/CXCL1, connective tissue-activating peptide-III (CTAP-III)/CXCL7, granulocyte chemotactic protein-2/CXCL6, IP-10/CXCL10, PF4/CXCL4, monokine induced by IFN-? | |||||||||||||||
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This conclusion is supported, at least in part, by the results of Sukumaran and colleagues [52], who reported the upregulated expression of chemokine genes encoding CXCL1, CXCL2, CXCL3, CXCL8, CCL3, CCL4 and CCL20 after infection of PMN with Anaplasma phagocytophilum. | |||||||||||||||
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The disparity in angiogenic activity among CXC chemokine family members is attributed to three amino acid structural domains at the N terminus, Glu-Leu-Arg (ELR), which is present in angiogenic (i.e., CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, and CXCL8) [4-6], but not angiostatic (i.e., CXCL4, CXCL9, CXCL10, and CXCL11) CXC chemokines [7]. | |||||||||||||||
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CXCL6 also has angiogenesis activity and can stimulate cancer cell progression.26,27 Zhu et al reported overexpression of CXCL6 with its receptor, IL8R, in hypoxic small cell lung cancer, which is an autocrine regulation for cell progression.28 Rubie et al observed an overexpression of CXCL1 and CXCL5 in CRC, but the level of CXCL6 was not changed.29 Our observations showed that copy number loss and low expression levels were correlated with the invasiveness of CRC. | |||||||||||||||
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Increases in gene expression of IL-8, GRO-alpha, MCP-1, and RANTES in response to TNF-alpha treatment were detected. | |||||||||||||||
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As observed above, ICAM-1, IL-6, IL-8, GM-CSF, RANTES, MCP-1, GROalpha, NAP-2, and ENA-78 expression was reduced by the IKK inhibitors. | |||||||||||||||
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IL33 rapidly induced the phosphorylation of MAPKs and IkappaBalpha, and enhanced the expression of inflammatory mediators (IL6, IL8, IP-10, Gro-alpha, Gro-beta and MCP-1) in IL4- or IFNgamma-pretreated cells. | |||||||||||||||
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