Linked Life Data

10331420

Source:http://linkedlifedata.com/resource/pubmed/id/10331420

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-5-27
pubmed:abstractText
Vascular endothelial growth factor (VEGF) has been suggested to play a role in the pathogenesis of diabetic vascular complications. In the present study, we investigated whether expression of monocyte chemoattractant protein-1 (MCP-1), a chemokine that has been proposed to recruit leukocytes to sites of inflammation, neovascularization, and vascular injury, can be modulated by VEGF in bovine retinal microvascular endothelial cells (BRECs). VEGF induced expression of MCP-1 mRNA in BRECs in a concentration- and time-dependent manner. Secretion of MCP-1 into the culture medium of BRECs treated with VEGF for 24 h was increased by 2.2-fold compared with the control. Inhibitors of transcription factor NF-kappaB, N-alpha-tosyl-L-lysine chloromethylketone (TLCK) and N-acetylcysteine (NAC), as well as an inhibitor of the extracellular signal-regulated kinase (ERK) pathway, PD 98059, attenuated VEGF-induced expression of MCP-1 mRNA. Using electrophoretic gel mobility shift assay, we observed that VEGF stimulated binding activity of NF-kappaB. VEGF-induced NF-kappaB activation was inhibited by TLCK and NAC, but not by PD 98059. Binding activity of transcription factor AP-1, which is suggested to regulate induction of the MCP-1 gene together with NF-kappaB, was also stimulated by VEGF. PD 98059 inhibited the VEGF-induced activation of AP-1. These results indicate that VEGF induces MCP-1 expression in BRECs most likely by activating NF-kappaB and AP-1 via ERK-independent and -dependent pathways. Activation of NF-kappaB and induction of MCP-1 by VEGF in microvascular endothelial cells may contribute to the development of diabetic vascular complications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1131-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10331420-Acetylcysteine, pubmed-meshheading:10331420-Animals, pubmed-meshheading:10331420-Cattle, pubmed-meshheading:10331420-Chemokine CCL2, pubmed-meshheading:10331420-Endothelial Growth Factors, pubmed-meshheading:10331420-Endothelium, Vascular, pubmed-meshheading:10331420-Gene Expression, pubmed-meshheading:10331420-Kinetics, pubmed-meshheading:10331420-Lymphokines, pubmed-meshheading:10331420-Microcirculation, pubmed-meshheading:10331420-NF-kappa B, pubmed-meshheading:10331420-RNA, Messenger, pubmed-meshheading:10331420-Retinal Vessels, pubmed-meshheading:10331420-Tosyllysine Chloromethyl Ketone, pubmed-meshheading:10331420-Transcription Factor AP-1, pubmed-meshheading:10331420-Vascular Endothelial Growth Factor A, pubmed-meshheading:10331420-Vascular Endothelial Growth Factors
pubmed:year
1999
pubmed:articleTitle
Vascular endothelial growth factor activates nuclear factor-kappaB and induces monocyte chemoattractant protein-1 in bovine retinal endothelial cells.
pubmed:affiliation
Institut für Kardiovaskuläre Physiologie, Klinikum der Johann Wolfgang Goethe Universität, Frankfurt am Main, Germany. r.busse@em.uni-frankfurt.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't