Linked Life Data

9313759

Source:http://linkedlifedata.com/resource/pubmed/id/9313759

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1997-10-30
pubmed:abstractText
Insulin-like growth factor I (IGF-I) and vascular endothelial growth factor (VEGF) levels are correlated with retinal ischemia-associated intraocular neovascularization in humans. Since VEGF is required for iris and retinal neovascularization in animal models of retinal ischemia, we tested whether IGF-I could act as an indirect angiogenic factor by increasing VEGF gene expression. IGF-I increased retinal pigment epithelial (RPE) cell VEGF mRNA in a concentration-dependent manner with an EC50 of 7 nmol/1 (53.6 ng/ml). RPE and bovine smooth muscle cells exposed to 50 nmol/l (383 ng/m1) IGF-I achieved peak VEGF mRNA expression within 2 h. IGF-I-treated RPE cells increased VEGF protein levels in conditioned media and stimulated capillary endothelial cell proliferation. Blockade of the IGF-I receptor with a neutralizing antibody abrogated the VEGF increases in RPE cells. Further, hypoxia-mediated and IGF-I-mediated increases in VEGF mRNA and protein levels were additive in RPE cells, and the hypoxia-induced VEGF increases were independent of endogenous IGF-I. VEGF promoter activity was enhanced by IGF-I in RPE cells, but VEGF transcript half-life was unaltered. In summary, the supplementation of RPE and smooth muscle cell cultures with IGF-I at 5-100 nmol/l increased VEGF mRNA and secreted protein levels. The VEGF increases in RPE cells occurred primarily through enhanced transcription of the VEGF gene and via the IGF-I receptor. Elevated IGF-I levels may promote neovascularization through increased retinal VEGF gene expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1619-26
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9313759-Animals, pubmed-meshheading:9313759-Antibodies, pubmed-meshheading:9313759-Blotting, Northern, pubmed-meshheading:9313759-Capillaries, pubmed-meshheading:9313759-Cell Division, pubmed-meshheading:9313759-Cell Hypoxia, pubmed-meshheading:9313759-Cell Line, Transformed, pubmed-meshheading:9313759-Culture Media, Conditioned, pubmed-meshheading:9313759-Endothelial Growth Factors, pubmed-meshheading:9313759-Endothelium, Vascular, pubmed-meshheading:9313759-Gene Expression Regulation, pubmed-meshheading:9313759-Humans, pubmed-meshheading:9313759-Insulin-Like Growth Factor I, pubmed-meshheading:9313759-Kinetics, pubmed-meshheading:9313759-Lymphokines, pubmed-meshheading:9313759-Mice, pubmed-meshheading:9313759-Pigment Epithelium of Eye, pubmed-meshheading:9313759-Promoter Regions, Genetic, pubmed-meshheading:9313759-RNA, Messenger, pubmed-meshheading:9313759-Receptor, IGF Type 1, pubmed-meshheading:9313759-Vascular Endothelial Growth Factor A, pubmed-meshheading:9313759-Vascular Endothelial Growth Factors
pubmed:year
1997
pubmed:articleTitle
Regulation of vascular endothelial growth factor expression by insulin-like growth factor I.
pubmed:affiliation
Laboratory for Surgical Research, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't