Enterostatin inhibition of angiogenesis: possible role of pAMPK and vascular endothelial growth factor A (VEGF-A) View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-02-26

AUTHORS

M Park, J Lyons, H Oh, Y Yu, E A Woltering, F Greenway, D A York

ABSTRACT

Introduction:We utilized a genomic analysis of the response of neuronal GT1-7 cells to enterostatin to identify pathways responsive to this peptide. This information, together with reported properties of the enterostatin receptor, suggested that enterostatin may have an effect on angiogenesis.Method:To investigate this hypothesis, we studied the effect of enterostatin as an antiangiogenic agent in two angiogenic tissue culture model systems.Results:Enterostatin induced a 50% or greater inhibition in the angiogenic response of human fat cells and had a U-shaped bimodal dose–response effect in inhibiting angiogenesis in a human placental vein angiogenesis model. To further understand this response, we tested enterostatin's effect in a human hepatoma cell line (HepG2 cells) that was subjected to glucose deprivation, a condition known to induce angiogenesis in other tumor cell lines. Phosphorylated AMP kinase (pAMPK) levels and vascular endothelial growth factor A (VEGF-A) mRNA expression were elevated robustly after incubation of HepG2 cells in the absence of glucose for 4 h, but 15 min incubation with enterostatin dramatically inhibited this pAMPK activation and reduced VEGF-A gene expression after 1 h incubation with enterostatin. The AMPK activator 5-aminoimidazole-4-carboximide ribonucleoside (AICAR) induced VEGF-A expression.Summary:These data suggest that enterostatin has an antiangiogenic effect and suggest that it regulates VEGF-A gene expression through inhibition of AMPK activity. More... »

PAGES

922-929

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ijo.2008.16

DOI

http://dx.doi.org/10.1038/ijo.2008.16

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031593522

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18301390


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