title: Anti-mullerian hormone is expressed by endometriosis tissues and induces cell cycle arrest and apoptosis in endometriosis cells.
abstract: BACKGROUND
  The anti-mullerian hormone (AMH) is a member of the transforming growth factor β (TGF-β) superfamily, which is responsible of the regression of the mullerian duct. AMH is expressed in the normal endometrium, where, acting in a paracrine fashion, negatively regulates cellular viability. Our objective was to evaluate the in vitro effects of the treatment with AMH of endometriosic cells.
  
  
  METHODS
  AMH expression in human endometriosis glands was evaluated by immunohistochemistry. RT-PCR has been used to quantify the expression levels of AMH and AMH RII isoforms, as well as of cytochrome P450 in both endometriosis epithelial and stromal cells Effects of AMH and AMH-cleaved treatment in endometriosis cells were evaluated by flow-cytometry analysis. Finally, it has been evaluated the effect of plasmin-digested AMH on cytochrome P450 activity.
  
  
  RESULTS
  AMH and AMH RII isoforms, as well as cytochrome P450, were expressed in both endometriosis epithelial and stromal cells. Treatment of endometriosis stromal and epithelial cell growth with AMH was able to induce a decrease in the percentage of cells in S phase and increase percentage of cells in G1 and G2 phase; coherently, decreased cell viability and increased percentage of cells death fraction was observed. The plasmin-digested AMH was able to suppress most of the cytochrome P450 activity, causing an increase of pre-G1 phase and of apoptosis induction treating with plasmin-digested AMH in both cell lines, most marked in the epithelial cells.
  
  
  CONCLUSIONS
  The data produced suggest a possible use of AMH as therapeutic agents in endometriosis.
authors.affiliation: Centro Italiano Endometriosi, Via Aurelia, 559, Rome 00165, Italy. research@endometriosi.it.
authors.forename: Pietro G
authors.initials: PG
authors.lastname: Signorile
authors.forename: Francesca
authors.initials: F
authors.lastname: Petraglia
authors.forename: Alfonso
authors.initials: A
authors.lastname: Baldi
mesh_terms: D054304:Anti-Mullerian Hormone / Q000737:chemistry / Q000494:pharmacology / Q000502:physiology*; D017209:Apoptosis; D059447:Cell Cycle Checkpoints; D049109:Cell Proliferation; D002470:Cell Survival; D002478:Cells, Cultured; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004715:Endometriosis / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005341:Fibrinolysin / Q000737:chemistry; D006801:Humans; D010446:Peptide Fragments / Q000737:chemistry / Q000494:pharmacology; D059748:Proteolysis; D018000:Receptors, Peptide / Q000378:metabolism; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D010446:Peptide Fragments; D018000:Receptors, Peptide; D018125:Receptors, Transforming Growth Factor beta; C084621:anti-Mullerian hormone receptor; D054304:Anti-Mullerian Hormone; D003577:Cytochrome P-450 Enzyme System; D005341:Fibrinolysin