Source:http://linkedlifedata.com/resource/pubmed/id/16356505
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0109317,
umls-concept:C0185117,
umls-concept:C0441712,
umls-concept:C0443616,
umls-concept:C0752312,
umls-concept:C1150579,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1370600,
umls-concept:C1539081,
umls-concept:C1704259,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1705987,
umls-concept:C2911684
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| pubmed:issue |
2
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| pubmed:dateCreated |
2006-7-4
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| pubmed:abstractText |
CD40 is a 48kDa phosphorylated transmembrane glycoprotein that belongs to the tumor necrosis factor receptor superfamily and may play a role in formation of atherosclerotic plaques. Here, we investigated the effect of chylomicron remnants on CD40 expression in the human premonocytic cell line, THP-1 cells. Chylomicron remnants upregulated the expression of CD40 protein and mRNA in a dose- and time-dependent manner. Further, chylomicron remnants increased the generation of reactive oxygen species as determined by an increasing level of 2',7'-dichlorofluorescein. Pretreatment with the antioxidant, N-acetylcysteine, inhibited chylomicron remnant-induced CD40 protein expression by 60%. On the other hand, chylomicron remnants transiently increased the phosphorylation of extracellular signal-regulated kinase (ERK 1/2) and p38 mitogen-activated protein kinase (MAPK). Pretreatment with the MAPK kinase inhibitor, U0126, completely inhibited chylomicron remnants-induced CD40 protein expression, whereas the p38 MAPK inhibitor, SB203580, had no effect. Pretreatment with N-acetylcysteine had no effect on chylomicron remnant-induced ERK 1/2 phosphorylation. These data suggest that CD40 expression stimulated by chylomicron remnants in THP-1 cells is dependent on ERK 1/2-mediated pathway, which is followed by redox-sensitive mechanism-dependent and independent pathway. Thus, chylomicron remnants may contribute to the formation of atherosclerotic plaques via their immunological and proinflammatory effects.
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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/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Chylomicron Remnants,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
0021-9150
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
187
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
257-64
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:16356505-Animals,
pubmed-meshheading:16356505-Antigens, CD40,
pubmed-meshheading:16356505-Atherosclerosis,
pubmed-meshheading:16356505-Cell Line,
pubmed-meshheading:16356505-Chylomicron Remnants,
pubmed-meshheading:16356505-Gene Expression Regulation,
pubmed-meshheading:16356505-Humans,
pubmed-meshheading:16356505-MAP Kinase Signaling System,
pubmed-meshheading:16356505-Male,
pubmed-meshheading:16356505-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:16356505-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:16356505-Monocytes,
pubmed-meshheading:16356505-Oxidation-Reduction,
pubmed-meshheading:16356505-Rats,
pubmed-meshheading:16356505-Rats, Sprague-Dawley,
pubmed-meshheading:16356505-Reactive Oxygen Species,
pubmed-meshheading:16356505-Up-Regulation,
pubmed-meshheading:16356505-Vasculitis,
pubmed-meshheading:16356505-p38 Mitogen-Activated Protein Kinases
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| pubmed:year |
2006
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| pubmed:articleTitle |
Chylomicron remnants upregulate CD40 expression via the ERK pathway and a redox-sensitive mechanism in THP-1 cells.
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| pubmed:affiliation |
Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
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| pubmed:publicationType |
Journal Article
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