title: Soluble factors from human endometrium promote angiogenesis and regulate the endothelial cell transcriptome.
abstract: BACKGROUND
  Angiogenesis and vascular remodeling play critical roles in the cyclical growth and regression of endometrium. They also appear to play roles in the pathogenesis of endometriosis.
  
  
  RESULTS
  Supernatants were collected from cultured endometrium isolated from women with and without endometriosis. These supernatants induced endothelial cell proliferation and angiogenesis in vitro. They contained vascular endothelial growth factor (VEGF)-A, and their proliferative effects on endothelial cells were partially abrogated by a blocking anti-VEGF-A antibody. Gene array analysis showed that culture supernatants from proliferative phase endometrium, and to a lesser extent secretory phase endometrium, induced significant changes in the transcriptome of endothelial cells. We could not detect any association between endometriosis and the ability of endometrial-derived soluble factors to promote angiogenesis or to regulate the endothelial transcriptome. In addition, we could not detect any association between endometriosis and the concentration of VEGF-A in supernatants from cultured endometrium or in menstrual effluent.
  
  
  CONCLUSIONS
  We have shown that endometrium cultured in vitro produced soluble factors, including VEGF-A, that promoted angiogenesis. Proliferative phase endometrium promoted significant endothelial cell transcriptome changes that appear overall to be pro-angiogenic. These transcriptome changes provide insight into the dynamic control of vessel structure on which both eutopic endometrium and endometriotic lesions depend.
authors.affiliation: Department of Pathology, Cambridge University, Tennis Court Road, Cambridge, CB2 1QP, UK. cgp22@cam.ac.uk
authors.forename: Cristin
authors.initials: C
authors.lastname: Print
authors.forename: Reija
authors.initials: R
authors.lastname: Valtola
authors.forename: Amanda
authors.initials: A
authors.lastname: Evans
authors.forename: Khashayar
authors.initials: K
authors.lastname: Lessan
authors.forename: Shazia
authors.initials: S
authors.lastname: Malik
authors.forename: Stephen
authors.initials: S
authors.lastname: Smith
mesh_terms: D016022:Case-Control Studies; D002455:Cell Division / Q000187:drug effects; D003470:Culture Media / Q000737:chemistry / Q000494:pharmacology; D004715:Endometriosis / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D004717:Endometrium / Q000098:blood supply* / Q000378:metabolism / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology*; D005260:Female; D005498:Follicular Phase; D006801:Humans; D009389:Neovascularization, Pathologic / Q000209:etiology; D018919:Neovascularization, Physiologic / Q000187:drug effects; D046509:Tissue Culture Techniques; D014158:Transcription, Genetic / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D003470:Culture Media; D042461:Vascular Endothelial Growth Factor A