title: Abnormal expression of the angiopoietins and Tie receptors in menorrhagic endometrium.
abstract: OBJECTIVE
  To identify changes in expression of stimulatory and inhibitory factors when normal endometrium becomes menorrhagic.
  
  
  METHODS
  Retrospective blinded immunohistologic study.
  
  
  METHODS
  Private research center.
  
  
  METHODS
  Premenopausal and postmenopausal women with non-menorrhagic and menorrhagic endometrium undergoing curettage or hysterectomy were selected.
  
  
  METHODS
  Samples of endometrium were obtained from all patients.
  
  
  METHODS
  Expression of angiopoietins 1 and 2, and vascular receptors Tie-1 and Tie-2 and endothelial nitric oxide synthase (eNOS).
  
  
  RESULTS
  Angiopoietin 1 (ANG-1) expression was similar in non-menorrhagic and menorrhagic endometrium. However, there was a significant increase in expression of ANG-2 and its receptor Tie-2 in menorrhagic tissues, which may be important in destabilizing the endometrial vasculature. Tie-1, responsible for endothelial integrity, was also increased in menorrhagic tissues, and is a likely compensatory mechanism for the existing vascular pathology. Expression of eNOS was also increased in menorrhagic women.
  
  
  CONCLUSIONS
  Differences in the expression of ANG-2, Tie-2, Tie-1, and eNOS were found in menorrhagic endometrium, which may represent a new target for therapeutic intervention to correct menorrhagic conditions.
authors.affiliation: Garden State Cancer Center, Belleville, New Jersey 07109, USA. rblumenthal@gscancer.org
authors.forename: Rosalyn D
authors.initials: RD
authors.lastname: Blumenthal
authors.forename: Alice P
authors.initials: AP
authors.lastname: Taylor
authors.forename: Lisa
authors.initials: L
authors.lastname: Goldman
authors.forename: Gloria
authors.initials: G
authors.lastname: Brown
authors.forename: David M
authors.initials: DM
authors.lastname: Goldenberg
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000378:metabolism*; D042683:Angiopoietin-1; D042702:Angiopoietin-2; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D005498:Follicular Phase / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008183:Luteal Phase / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism*; D008595:Menorrhagia / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D017698:Postmenopause / Q000378:metabolism; D017697:Premenopause / Q000378:metabolism; D011518:Proto-Oncogene Proteins; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D011956:Receptors, Cell Surface / Q000378:metabolism*; D042764:Receptors, TIE; D012189:Retrospective Studies
chemical_list: D043925:Angiogenesis Inducing Agents; D042683:Angiopoietin-1; D042702:Angiopoietin-2; C105373:MEN1 protein, human; D008562:Membrane Glycoproteins; D009363:Neoplasm Proteins; D011518:Proto-Oncogene Proteins; D011956:Receptors, Cell Surface; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D020794:Receptor Protein-Tyrosine Kinases; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D042764:Receptors, TIE