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Title: | Effect of angiogenesis inhibitors on oestrogen-mediated endometrial endothelial cell proliferation in the ovariectomized mouse. | Authors: | Lipson K.E.;Rogers P.A.W.;Heryanto B. | Institution: | (Heryanto, Rogers) Centre for Women's Health Research, Monash Univ. Dept. Obstet./Gynaecol., Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia (Lipson) SUGEN Inc., 230 East Grand Avenue, South San Francisco, CA 94080, United States | Issue Date: | 19-Oct-2012 | Copyright year: | 2003 | Publisher: | BioScientifica Ltd. (Euro House, 22 Apex Court, Woodlands, Bradley Stoke, Bristol BS32 4JT, United Kingdom) | Place of publication: | United Kingdom | Publication information: | Reproduction. 125 (3) (pp 337-346), 2003. Date of Publication: 01 Mar 2003. | Abstract: | It has been suggested that endometrial angiogenesis in response to the sex steroids oestrogen and progesterone is mediated at a local level via compounds such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF), acting through their respective tyrosine kinase receptors. The aim of the present study was to use SUGEN tyrosine kinase receptor angiogenic inhibitor compounds SU5416, SU5402, SU11652 and SU11685, to determine whether VEGF, FGF or PDGF play a role in mediating endometrial endothelial cell proliferation after administration of oestrogen and progesterone. Endometrial endothelial cell proliferation was induced in adult ovariectomized mice by either oestrogen alone for 24 h (E1), or a regimen using oestrogen alone, then progesterone with low dose oestrogen, followed by progesterone with high-dose oestrogen (PE) over a total of 7 days. Each angiogenesis inhibitor compound was injected daily for 4 days (100 mg kg-1 day-1, s.c.) before endometrial tissue collection at either the E1 or PE stage. This study also evaluated the effect of VEGF antiserum (0.2 ml, i.p.) on endothelial cell proliferation at the E1 stage. All four angiogenic inhibitor compounds significantly reduced endothelial cell proliferation activity at the E1 and PE stages. The greatest reduction in the endothelial cell proliferative index was at the E1 stage in the group treated with the VEGF receptor inhibitor SU5416 (2.5 +/- 0.7% versus 27.9 +/- 1.1%, P < 0.001), with a reduction of similar magnitude in the group treated with anti-VEGF antibody. At the PE stage, all four inhibitors significantly reduced endothelial cell proliferation to a similar extent, indicating that VEGF, FGF and PDGF are all involved. These results demonstrate that endometrial angiogenesis after acute oestrogen treatment is primarily mediated by VEGF, but that under the influence of combined oestrogen and progesterone, FGF and PDGF are also probably involved. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1530/rep.0.1250337 | PubMed URL: | 12611597 [http://www.ncbi.nlm.nih.gov/pubmed/?term=12611597] | ISSN: | 1470-1626 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/32708 | Type: | Review | Subjects: | female hormone action hormone response mouse nonhuman *ovariectomy priority journal review time 2 butanone 3 [4 methyl 2 (2 oxo 3 indolinylmethylidenyl) 3 pyrrolyl]propionic acid/cm [Drug Comparison] 3 [4 methyl 2 (2 oxo 3 indolinylmethylidenyl) 3 pyrrolyl]propionic acid/do [Drug Dose] 3 [4 methyl 2 (2 oxo 3 indolinylmethylidenyl) 3 pyrrolyl]propionic acid/pd [Pharmacology] 3 [4 methyl 2 (2 oxo 3 indolinylmethylidenyl) 3 pyrrolyl]propionic acid/sc [Subcutaneous Drug Administration] anesthetic agent *angiogenesis inhibitor/cm [Drug Comparison] *angiogenesis inhibitor/do [Drug Dose] *angiogenesis inhibitor/pd [Pharmacology] *angiogenesis inhibitor/sc [Subcutaneous Drug Administration] arachis oil bromethol *estrogen/cb [Drug Combination] *estrogen/do [Drug Dose] *estrogen/pd [Pharmacology] fibroblast growth factor/ec [Endogenous Compound] platelet derived growth factor/ec [Endogenous Compound] progesterone/cm [Drug Comparison] progesterone/pd [Pharmacology] pyrrole derivative/cm [Drug Comparison] pyrrole derivative/do [Drug Dose] pyrrole derivative/pd [Pharmacology] pyrrole derivative/sc [Subcutaneous Drug Administration] receptor blocking agent/cm [Drug Comparison] receptor blocking agent/do [Drug Dose] receptor blocking agent/pd [Pharmacology] receptor blocking agent/sc [Subcutaneous Drug Administration] semaxanib/cm [Drug Comparison] semaxanib/do [Drug Dose] semaxanib/pd [Pharmacology] semaxanib/sc [Subcutaneous Drug Administration] sex hormone/cb [Drug Combination] sex hormone/do [Drug Dose] sex hormone/pd [Pharmacology] sodium chloride tyrosine kinase receptor/ec [Endogenous Compound] unclassified drug vasculotropin/ec [Endogenous Compound] vasculotropin antibody/cb [Drug Combination] vasculotropin antibody/cm [Drug Comparison] vasculotropin antibody/do [Drug Dose] vasculotropin antibody/ip [Intraperitoneal Drug Administration] vasculotropin antibody/pd [Pharmacology] su 11652/cm [Drug Comparison] su 11652/do [Drug Dose] su 11652/pd [Pharmacology] su 11652/sc [Subcutaneous Drug Administration] su 11685/cm [Drug Comparison] su 11685/do [Drug Dose] su 11685/pd [Pharmacology] su 11685/sc [Subcutaneous Drug Administration] low drug dose age angiogenesis animal cell animal experiment animal tissue cell activity cell cycle cell proliferation controlled study dose response drug effect drug mechanism *endometrium cell *endothelium cell estrogen therapy drug mechanism *endometrium cell *endothelium cell estrogen therapy female hormone action hormone response low drug dose mouse nonhuman animal cell priority journal review time angiogenesis age *ovariectomy animal experiment animal tissue cell activity cell cycle cell proliferation controlled study dose response drug effect |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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