title: DFF45 expression in ovarian endometriomas.
abstract: OBJECTIVE
  Endometriosis, defined as a spread of endometrium outside the uterus cavity, affects up to 30% women of reproductive age, with the ovaries being its most common localization. In the ectopic lesions, endometrial cells show abnormal proliferation and impaired apoptosis. The DNA destruction during apoptosis is a direct result of activation of the DFF40/DFF45 complex. DFF40 (DNA fragmentation factor of 40 kDa) is responsible for direct DNA fragmentation while DFF45 (DNA fragmentation factor of 45 kDa) acts not only as a DFF40 inhibitor, but also as its chaperone. Therefore, the presence of DFF45 is required for proper DFF40 synthesis. The aim of this study was to determine the DFF45 level in human ovarian endometriosis.
  
  
  METHODS
  The endometriosis samples were collected from 43 affected women, while the 81 normal endometrial specimens were obtained from the control group. Western blot and immunohistochemistry tests were used to determine the DFF45 level in examined tissues.
  
  
  RESULTS
  The expression of DFF45 in normal human endometrium and ovarian endometriosis was confirmed using both the Western blot and the immunohistochemistry tests. In normal eutopic proliferatory endometrium, a lower DFF45 expression was observed compared with secretory endometrium, while no cyclic changes in DFF45 expression were observed in the ovarian endometriomas. In the normal eutopic endometrium, stronger DFF45 staining was noted in the endometrial glands in comparison to the stroma, irrespective of menstrual cycle phase. However, in the ovarian endometriosis no difference between the glandular layer and stroma in DFF45 immunoreactivity was appreciated. The lowest level of DFF45 was observed in ovarian endometriosis when compared with both normal eutopic proliferatory and secretory endometria using the Western blot and immunohistochemistry analysis.
  
  
  CONCLUSIONS
  A decreased level of DFF45 observed in ovarian endometriosis may be a part of an apoptosis-resistant mechanism enhancing the disease progression.
authors.affiliation: Jagiellonian University, Chair of Obstetrics and Gynecology, 23 Kopernika Street, 30-501 Krakow, Poland. tbanas@mp.pl
authors.forename: Tomasz
authors.initials: T
authors.lastname: Banas
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Skotniczny
authors.forename: Antoni
authors.initials: A
authors.lastname: Basta
mesh_terms: D000328:Adult; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis*; D003851:Deoxyribonucleases / Q000037:antagonists & inhibitors; D004715:Endometriosis / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D006801:Humans; D008597:Menstrual Cycle / Q000502:physiology; D008875:Middle Aged
chemical_list: D051017:Apoptosis Regulatory Proteins; C109664:caspase-activated DNase inhibitor; D003851:Deoxyribonucleases