Linked Life Data

10698175

Source:http://linkedlifedata.com/resource/pubmed/id/10698175

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-3-16
pubmed:abstractText
Manipulation of angiogenesis may have a profound effect on female reproductive function, but this has not yet been demonstrated by direct experiment in species with ovulatory cycles similar to those in women. To investigate whether angiogenesis could be inhibited in the primate corpus luteum, and the consequences of such inhibition on luteal function, marmosets were treated with an antibody to vascular endothelial growth factor (VEGF). Treatment commenced at the time of ovulation and was continued for 3 days (early luteal group) or 10 days (midluteal group). Bromodeoxyuridine was used to label proliferating cells, being administered 1 h before collecting ovaries from control and treated animals in the early or midluteal phase. Ovarian sections were stained using an antibody to bromodeoxyuridine, and a proliferation index was obtained; endothelial cell quantification was performed using factor VIII as an endothelial cell marker. Intense proliferation in the early luteal phase was suppressed by anti-VEGF treatment. This resulted in blockade of development of the normally extensive capillary bed, as in the animals treated until the mid-luteal phase the numbers of endothelial cells were reduced. The hormone-producing cells remained largely unaltered in the posttreatment corpus luteum, although the presence of lipid accumulation, and small pockets of cells showing basophilia and nuclear condensation were observed. Significantly, luteal function, as judged by secretion of progesterone, was markedly compromised by the treatment, being reduced by 60% in comparison with controls. It is concluded that VEGF-mediated angiogenesis is an essential component of luteal function in primates and therefore has the potential to be regulated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
141
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
995-1000
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10698175-Animals, pubmed-meshheading:10698175-Antibodies, Blocking, pubmed-meshheading:10698175-Antimetabolites, pubmed-meshheading:10698175-Bromodeoxyuridine, pubmed-meshheading:10698175-Callithrix, pubmed-meshheading:10698175-Cell Division, pubmed-meshheading:10698175-Corpus Luteum, pubmed-meshheading:10698175-Endothelial Growth Factors, pubmed-meshheading:10698175-Endothelium, Vascular, pubmed-meshheading:10698175-Female, pubmed-meshheading:10698175-Immunohistochemistry, pubmed-meshheading:10698175-Lymphokines, pubmed-meshheading:10698175-Neovascularization, Physiologic, pubmed-meshheading:10698175-Organ Size, pubmed-meshheading:10698175-Ovary, pubmed-meshheading:10698175-Progesterone, pubmed-meshheading:10698175-Regional Blood Flow, pubmed-meshheading:10698175-Time Factors, pubmed-meshheading:10698175-Vascular Endothelial Growth Factor A, pubmed-meshheading:10698175-Vascular Endothelial Growth Factors
pubmed:year
2000
pubmed:articleTitle
Suppression of luteal angiogenesis in the primate after neutralization of vascular endothelial growth factor.
pubmed:affiliation
Medical Research Council Reproductive Biology Unit, Center for Reproductive Biology, Edinburgh, United Kingdom. h.fraser@ed-rbu.mrc.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't