Document Detail


Patterns of expression of vascular endothelial growth factor (VEGF) and VEGF receptors in mice suggest a role in hormonally regulated angiogenesis.
MedLine Citation:
PMID:  7683699     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vascular endothelial growth factor (VEGF) is a secreted endothelial cell-specific mitogen. To evaluate whether VEGF may play a role in angiogenesis, we have determined the spatial and temporal patterns of expression of VEGF and VEGF receptors during natural angiogenic processes taking place within the female reproductive system. Four angiogenic processes were analyzed: neovascularization of ovarian follicles, neovascularization of the corpus luteum, repair of endometrial vessels, and angiogenesis in embryonic implantation sites. During all processes, VEGF mRNA was found to be expressed in cells surrounding the expanding vasculature. VEGF was predominantly produced in tissues that acquire new capillary networks (theca layers, lutein cells, endometrial stroma, and the maternal decidua, respectively). VEGF-binding activity, on the other hand, was found on endothelial cells of both quiescent and proliferating blood vessels. These findings are consistent with a role for VEGF in the targeting of angiogenic responses to specific areas. Using in situ hybridization, we show that VEGF is expressed in 10 different steroidogenic and/or steroid-responsive cell types (theca, cumulus, granulosa, lutein, oviductal epithelium, endometrial stroma, decidua, giant trophoblast cells, adrenal cortex, and Leydig cells). Furthermore, in some cells upregulation of VEGF expression is concurrent with the acquisition of steroidogenic activity, and expression in other cell types is restricted to a particular stage of the ovarian cycle. These findings suggest that expression of VEGF is hormonally regulated. We propose that excessive expression of VEGF during gonadotropin-induced ovulation may contribute to the development of ovarian hyperstimulation syndromes by virtue of the vascular permeabilization activity of this factor.
Authors:
D Shweiki; A Itin; G Neufeld; H Gitay-Goren; E Keshet
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  91     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1993 May 
Date Detail:
Created Date:  1993-06-04     Completed Date:  1993-06-04     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2235-43     Citation Subset:  AIM; IM    
Affiliation:
Department of Molecular Biology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
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MeSH Terms
Descriptor/Qualifier:
Animals
Binding Sites
Embryo Implantation
Endometrium / blood supply,  physiology
Endothelial Growth Factors / genetics*,  metabolism
Fallopian Tubes / blood supply,  physiology*
Female
In Situ Hybridization
Lymphokines / genetics*,  metabolism
Male
Mice
Mice, Inbred C57BL
Neovascularization, Pathologic / physiopathology*
Ovary / blood supply,  physiology*
Protein-Tyrosine Kinases / genetics*,  metabolism
RNA, Messenger / analysis,  metabolism
Rats
Receptors, Vascular Endothelial Growth Factor
Uterus / blood supply,  physiology*
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Chemical
Reg. No./Substance:
0/Endothelial Growth Factors; 0/Lymphokines; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.1/Receptors, Vascular Endothelial Growth Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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