title: Identification of multiple and distinct defects in prostaglandin biosynthetic pathways in eutopic and ectopic endometrium of women with endometriosis.
abstract: OBJECTIVE
  To investigate prostaglandin (PG) biosynthesis and catabolism pathways in eutopic and ectopic endometrium of women with endometriosis.
  
  
  METHODS
  Retrospective study.
  
  
  METHODS
  Human reproduction research laboratory.
  
  
  METHODS
  Forty-five women with endometriosis and 29 normal controls.
  
  
  METHODS
  Endometrial and endometriotic tissue samples were obtained during laparoscopic surgery.
  
  
  METHODS
  Cyclo-oxygenases (Coxs 1 and 2), PGE2 synthases (microsomal [m] PGES 1 and 2 and cytosolic [c] PGES), PGF2α synthases (aldoketoreductase [AKR]-1C3 and AKR-1B1), and the PG catabolic enzyme 15-hydroxyprostaglandin dehydrogenase messenger RNA expression by quantitative real-time polymerase chain reaction and protein localization by immunohistochemistry.
  
  
  RESULTS
  This study showed a marked increase in the key PG biosynthesis enzymes Cox-2, mPGES-1, mPGES-2, cPGES, and AKR-1C3 in ectopic endometrial tissue of women with endometriosis, particularly in the earliest and most active stages of the disease, without a noticeable change in the expression of the PG catabolic enzyme 15-hydroxyprostaglandin dehydrogenase. Meanwhile, the significant increase in rate-limiting Cox-2 expression upstream was correlated downstream by a significant stage- and cycle phase-dependent decrease in the terminal specific synthase mPGES-2, thereby revealing the presence of counter-regulatory mechanisms, which operate in the eutopic endometrium of women with endometrium but seem to be lacking in the ectopic implantation sites.
  
  
  CONCLUSIONS
  This study reveals for the first time multiple defects in PG biosynthesis pathways, which differ between eutopic intrauterine and ectopic endometrial tissues and may, owing to the wide spectrum of PG properties, contribute to the initial steps of endometrial tissue growth and development and have an important role to play in the pathogenesis and symptoms of this disease.
authors.affiliation: Endocrinologie de la Reproduction, Centre Hospitalier Universitaire de Québec, Hôpital Saint-François d'Assise, Faculté de Médecine, Université Laval, Québec, Canada.
authors.forename: Halima
authors.initials: H
authors.lastname: Rakhila
authors.forename: Cédric
authors.initials: C
authors.lastname: Carli
authors.forename: Marlène
authors.initials: M
authors.lastname: Daris
authors.forename: Madeleine
authors.initials: M
authors.lastname: Lemyre
authors.forename: Mathieu
authors.initials: M
authors.lastname: Leboeuf
authors.forename: Ali
authors.initials: A
authors.lastname: Akoum
mesh_terms: D000328:Adult; D004715:Endometriosis / Q000378:metabolism*; D004717:Endometrium / Q000002:abnormalities* / Q000378:metabolism*; D005260:Female; D006801:Humans; D009097:Multienzyme Complexes / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis*; D012189:Retrospective Studies; D015398:Signal Transduction
chemical_list: D009097:Multienzyme Complexes; D011453:Prostaglandins
keywords: Endometriosis; PGs; endometrium