Linked Life Data

15795939

Source:http://linkedlifedata.com/resource/pubmed/id/15795939

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-7-4
pubmed:abstractText
n-3 polyunsaturated fatty acids (PUFAs) have been shown to exert beneficial effects in the prevention of cardiovascular disease, inflammation, and on tumor growth. To investigate effects of PUFAs on proliferation and apoptosis in endothelial cells, we tested the n-3 PUFA docosahexaenoic acid (DHA) and the n-6 PUFA arachidonic acid (AA) in human umbilical vein endothelial cells (HUVEC). The mitochondrial membrane potential (MMP) and the production of reactive oxygen species were examined by flow cytometry. Phosphorylation of p53 or p38 MAP kinase, and total levels of p53 were measured by Western blot. DNA binding activity of p53 was analyzed with a TransAM transcription factor assay kit. Tube formation was assessed on Matrigel. In proliferating HUVEC, but not in confluent cells, DHA reduced cell viability and induced apoptosis, as demonstrated by increases in membrane leakage (propidium iodide (PI) staining), Annexin-V binding, sub G(1) phase in the cell cycle, and TUNEL-positive cells. AA had no effect on these parameters. In addition to a reduced MMP and increased reactive oxygen species, phosphorylation of p38 and p53 (serine 15) and impaired DNA binding of p53 were observed. There was no change in total levels of p53. The p38 inhibitor SB203580 had no effect on Annexin V binding. DHA also attenuated HUVEC tube formation. Taken together, DHA induces apoptosis in proliferating, but not in resting HUVEC, potentially via the phosphorylation of p53, resulting in decreased p53 DNA binding. The results suggest that anti-angiogenic effects of DHA may be due to induction of apoptosis in proliferating endothelial cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2005 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
204
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
881-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15795939-Apoptosis, pubmed-meshheading:15795939-Arachidonic Acid, pubmed-meshheading:15795939-Cell Proliferation, pubmed-meshheading:15795939-Cell Shape, pubmed-meshheading:15795939-Cells, Cultured, pubmed-meshheading:15795939-DNA, pubmed-meshheading:15795939-DNA Fragmentation, pubmed-meshheading:15795939-Docosahexaenoic Acids, pubmed-meshheading:15795939-Endothelial Cells, pubmed-meshheading:15795939-Enzyme Activation, pubmed-meshheading:15795939-Humans, pubmed-meshheading:15795939-Membrane Potentials, pubmed-meshheading:15795939-Mitochondria, pubmed-meshheading:15795939-Phosphoserine, pubmed-meshheading:15795939-Phosphotyrosine, pubmed-meshheading:15795939-Superoxides, pubmed-meshheading:15795939-Tumor Suppressor Protein p53, pubmed-meshheading:15795939-Umbilical Cord, pubmed-meshheading:15795939-p38 Mitogen-Activated Protein Kinases
pubmed:year
2005
pubmed:articleTitle
Docosahexaenoic acid induces apoptosis in proliferating human endothelial cells.
pubmed:affiliation
Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universität München, Germany. hkim@med.uni-muenchen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't