title: Endostatin inhibits the growth of endometriotic lesions but does not affect fertility.
abstract: OBJECTIVE
  To determine whether endometriosis can be treated with the angiogenesis inhibitor endostatin and the effect of this treatment on fertility and reproduction.
  
  
  METHODS
  Pharmacologic intervention in a surgically induced model of endometriosis and in female mice undergoing mating.
  
  
  METHODS
  Animal research facility.
  
  
  METHODS
  Eight-week-old, female C57BL/6 and SCID mice.
  
  
  METHODS
  After implantation of autologous endometrium, mice received endostatin or the vehicle-matched control for 4 weeks. For the reproductive function study, mice receiving endostatin or vehicle were mated and reproductive functions were observed.
  
  
  METHODS
  Growth of endometriotic lesions after 4 weeks of treatment; estrous cycling, corpus luteum formation, serum hormone levels, and mating time as fertility measures; and pregnancy rates, length of pregnancy, fetal vitality, number, and outcome of litter as reproductive measures.
  
  
  RESULTS
  Endostatin suppressed the growth of endometriotic lesions by 47% compared with controls. Estrous cycling and corpus luteum formation were normal in both groups. Female mice receiving endostatin were as fertile as mice receiving vehicle, had normal pregnancies, and delivered the same number of pups. The offspring were healthy without teratogenic stigmata and reproduced normally themselves.
  
  
  CONCLUSIONS
  Antiangiogenic therapy with endostatin may present a promising novel, nontoxic therapeutic option for patients with endometriosis.
authors.affiliation: Department of Surgery, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Christian M
authors.initials: CM
authors.lastname: Becker
authors.forename: David A
authors.initials: DA
authors.lastname: Sampson
authors.forename: Maria A
authors.initials: MA
authors.lastname: Rupnick
authors.forename: Richard M
authors.initials: RM
authors.lastname: Rohan
authors.forename: Jason A
authors.initials: JA
authors.lastname: Efstathiou
authors.forename: Sarah M
authors.initials: SM
authors.lastname: Short
authors.forename: George A
authors.initials: GA
authors.lastname: Taylor
authors.forename: Judah
authors.initials: J
authors.lastname: Folkman
authors.forename: Robert J
authors.initials: RJ
authors.lastname: D'Amato
mesh_terms: D020533:Angiogenesis Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D000818:Animals; D045744:Cell Line, Tumor; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology*; D043169:Endostatins / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D005298:Fertility / Q000187:drug effects* / Q000502:physiology; D006131:Growth Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016513:Mice, SCID; D011247:Pregnancy
chemical_list: D020533:Angiogenesis Inhibitors; D043169:Endostatins; D006131:Growth Inhibitors