rdf:type |
|
lifeskim:mentions |
umls-concept:C0006560,
umls-concept:C0007634,
umls-concept:C0017262,
umls-concept:C0021469,
umls-concept:C0023688,
umls-concept:C0034634,
umls-concept:C0162574,
umls-concept:C0185117,
umls-concept:C0286651,
umls-concept:C0333348,
umls-concept:C0597357,
umls-concept:C1280500,
umls-concept:C1366622,
umls-concept:C2911684
|
pubmed:issue |
3
|
pubmed:dateCreated |
2010-7-19
|
pubmed:abstractText |
Receptor for advanced glycation end products (RAGE) may play an important role in inflammatory processes and endothelial activation. Extracellular newly identified RAGE binding protein (EN-RAGE), natural pro-inflammatory ligand for RAGE. The role of C-reactive protein (CRP) as a mediator in inflammation and atherosclerosis is the subject of recent investigations worldwide. In the present study, we investigated the effect of CRP on RAGE and EN-RAGE gene expression in THP-1 monocytic cell line. MAP kinases (ERK, p38 and JNK) were exploited as possible signaling pathways involved in the signal transduction by CRP. Further, atorvastatin was used as a therapeutic modality for modulation of these genes in the presence of CRP.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/C-Reactive Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Glycosylation End Products, Advanced,
http://linkedlifedata.com/resource/pubmed/chemical/Heptanoic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxymethylglutaryl-CoA...,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrroles,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/S100 Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/S100A12 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/advanced glycosylation end-product...,
http://linkedlifedata.com/resource/pubmed/chemical/atorvastatin,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jul
|
pubmed:issn |
1874-1754
|
pubmed:author |
|
pubmed:copyrightInfo |
Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:day |
23
|
pubmed:volume |
142
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
273-8
|
pubmed:meshHeading |
pubmed-meshheading:19201044-C-Reactive Protein,
pubmed-meshheading:19201044-Cell Division,
pubmed-meshheading:19201044-Cell Line, Tumor,
pubmed-meshheading:19201044-Cell Survival,
pubmed-meshheading:19201044-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:19201044-Gene Expression,
pubmed-meshheading:19201044-Glycosylation End Products, Advanced,
pubmed-meshheading:19201044-Heptanoic Acids,
pubmed-meshheading:19201044-Humans,
pubmed-meshheading:19201044-Hydroxymethylglutaryl-CoA Reductase Inhibitors,
pubmed-meshheading:19201044-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:19201044-MAP Kinase Signaling System,
pubmed-meshheading:19201044-Monocytes,
pubmed-meshheading:19201044-Pyrroles,
pubmed-meshheading:19201044-Receptors, IgG,
pubmed-meshheading:19201044-Receptors, Immunologic,
pubmed-meshheading:19201044-S100 Proteins,
pubmed-meshheading:19201044-Up-Regulation,
pubmed-meshheading:19201044-p38 Mitogen-Activated Protein Kinases
|
pubmed:year |
2010
|
pubmed:articleTitle |
C-reactive protein (CRP) up-regulates expression of receptor for advanced glycation end products (RAGE) and its inflammatory ligand EN-RAGE in THP-1 cells: inhibitory effects of atorvastatin.
|
pubmed:affiliation |
Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh 160012, India.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|