Source:http://linkedlifedata.com/resource/pubmed/id/15208668
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
39
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pubmed:dateCreated |
2004-8-26
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pubmed:abstractText |
Recent studies have suggested that the expression of interleukin-8 (IL-8) directly correlates with the vascularity of human gastric carcinomas. In this study, the effect of IL-1beta on IL-8 expression in human gastric cancer TMK-1 cells and the underlying signal transduction pathways were investigated. IL-1beta induced the IL-8 expression in a time- and concentration-dependent manner. IL-1beta induced the activation of extracellular signal-regulated kinases-1/2 and P38 mitogen-activated protein kinase (MAPK), but not the activation of c-jun amino-terminal kinse and Akt. Specific inhibitors of MEK-1 (PD980590) and P38 MAPK (SB203580) were found to suppress the IL-8 expression and the IL-8 promoter activity. Expression of vectors encoding a mutated-type MEK-1 and P38 MAPK resulted in decrease in the IL-8 promoter activity. IL-1beta also induced the production of reactive oxygen species (ROS). N-acetyl cysteine (NAC) prevented the IL-1beta-induced ROS production and IL-8 expression. In addition, exogenous H2O2 could induce the IL-8 expression. Deletional and site-directed mutagenesis studies on the IL-8 promoter revealed that activator protein-1 (AP-1) and nuclear factor (NF)-kappaB sites were required for the IL-1beta-induced IL-8 transcription. Electrophoretic mobility shift assay confirmed that IL-1beta increased the DNA-binding activity of AP-1 and NF-kappaB. Inhibitor (PD980590, SB203580) and ROS scavenger (NAC) studies revealed that the upstream signalings for the transcription factors AP-1 and NF-kappaB were MAPK and ROS, respectively. Conditioned media from the TMK-1 cells pretreated with IL-1beta could remarkably stimulate the in vitro growth of HUVEC and this effect was partially abrogated by IL-8-neutralizing antibodies. The above results suggest that MAPK-AP-1 and ROS-NF-kappaB signaling pathways are involved in the IL-1beta-induced IL-8 expression and that these paracrine signaling pathways induce endothelial cell proliferation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0950-9232
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pubmed:author |
pubmed-author:AhnBong WBW,
pubmed-author:EllisLee MLM,
pubmed-author:HwangYoung SYS,
pubmed-author:JeongMinM,
pubmed-author:JungYoung DYD,
pubmed-author:KimHyeong RHR,
pubmed-author:KimMi HMH,
pubmed-author:LeeDae BDB,
pubmed-author:MukaidaNaofumiN,
pubmed-author:ParkJung SJS,
pubmed-author:ShinBoo ABA
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pubmed:issnType |
Print
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pubmed:day |
26
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6603-11
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15208668-Cell Line, Tumor,
pubmed-meshheading:15208668-Culture Media, Conditioned,
pubmed-meshheading:15208668-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15208668-Humans,
pubmed-meshheading:15208668-Interleukin-1,
pubmed-meshheading:15208668-Interleukin-8,
pubmed-meshheading:15208668-Mitogen-Activated Protein Kinases,
pubmed-meshheading:15208668-RNA, Messenger,
pubmed-meshheading:15208668-Reactive Oxygen Species,
pubmed-meshheading:15208668-Signal Transduction,
pubmed-meshheading:15208668-Stomach Neoplasms
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pubmed:year |
2004
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pubmed:articleTitle |
Interleukin-1beta stimulates IL-8 expression through MAP kinase and ROS signaling in human gastric carcinoma cells.
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pubmed:affiliation |
Department of Biochemistry, Chonnam University Research Institute of Medical Sciences, Chonnam National University Medical School, 5 Hakdong, Kwangju, 501-190, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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