| pubmed-article:12732205 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12732205 | lifeskim:mentions | umls-concept:C1257792 | lld:lifeskim |
| pubmed-article:12732205 | lifeskim:mentions | umls-concept:C1120843 | lld:lifeskim |
| pubmed-article:12732205 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
| pubmed-article:12732205 | lifeskim:mentions | umls-concept:C2754810 | lld:lifeskim |
| pubmed-article:12732205 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:12732205 | pubmed:dateCreated | 2003-5-6 | lld:pubmed |
| pubmed-article:12732205 | pubmed:abstractText | In diabetes mellitus (DM), hyperglycemia causes cardiovascular lesions through endothelial dysfunction. Monocyte chemoattractant protein-1 (MCP-1) is implicated in the pathogenesis of cardiovascular lesions. By using human umbilical vein endothelial cells, we investigated the effect of hyperglycemia on MCP-1 production and its signaling pathways. Chronic incubation with high glucose increased mRNA expression and production rate of MCP-1 in a time (1-7 days)- and concentration (10-35 mM)-dependent manner. Chronic exposure to high glucose resulted in enhancement of generation of reactive oxygen species (ROS), as determined by increasing level of 2,7-dichlorofluorescein (DCF), and subsequent activation of p38 mitogen-activated protein kinase (MAPK). Neither c-Jun NH(2)-terminal kinase nor extracellular signal-regulated kinase1/2 was affected. SB203580 or FR167653, p38 MAPK specific inhibitors, completely suppressed MCP-1 expression. Catalase suppressed p38 MAPK phosphorylation and MCP-1 expression. These results indicate that hyperglycemia can accelerate MCP-1 production through the mechanism involving p38 MAPK, ROS-sensitive signaling pathway, in vascular endothelial cells. | lld:pubmed |
| pubmed-article:12732205 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12732205 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12732205 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12732205 | pubmed:month | May | lld:pubmed |
| pubmed-article:12732205 | pubmed:issn | 0006-291X | lld:pubmed |
| pubmed-article:12732205 | pubmed:author | pubmed-author:YokoyamaMitsu... | lld:pubmed |
| pubmed-article:12732205 | pubmed:author | pubmed-author:TakahashiAkih... | lld:pubmed |
| pubmed-article:12732205 | pubmed:author | pubmed-author:IshikawaYuich... | lld:pubmed |
| pubmed-article:12732205 | pubmed:author | pubmed-author:TaniguchiTaka... | lld:pubmed |
| pubmed-article:12732205 | pubmed:author | pubmed-author:TakaishiHiros... | lld:pubmed |
| pubmed-article:12732205 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12732205 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:12732205 | pubmed:volume | 305 | lld:pubmed |
| pubmed-article:12732205 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12732205 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12732205 | pubmed:pagination | 122-8 | lld:pubmed |
| pubmed-article:12732205 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:meshHeading | pubmed-meshheading:12732205... | lld:pubmed |
| pubmed-article:12732205 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12732205 | pubmed:articleTitle | High glucose accelerates MCP-1 production via p38 MAPK in vascular endothelial cells. | lld:pubmed |
| pubmed-article:12732205 | pubmed:affiliation | Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. | lld:pubmed |
| pubmed-article:12732205 | pubmed:publicationType | Journal Article | lld:pubmed |
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