title: The placental RCAS1 expression during stillbirth.
abstract: BACKGROUND
  Independently of the fetal death cause the beginning and course of stillbirth is closely related with the growing cytotoxic activity at the maternal-fetal interface. RCAS1 participates in the inhibition of maternal immune response during pregnancy. The alterations of RCAS1 protein expression in placental cells seem to determine the beginning of the labor and participate in the placental abruption. The aim of the present study was to investigate RCAS1 expression in placentas obtained following stillbirths or normal term births.
  
  
  METHODS
  RCAS1 expression was evaluated by Western blot method with the use of monoclonal anti-RCAS1 antibody in 67 placental tissue samples. Pregnant women were divided into four groups according to the mode of labor onset--spontaneous or induced, and the type of labor, stillbirth or labor at term. Placental beta-Actin expression was chosen as a control protein. Relative amounts of placental RCAS1 were compared with the use of Student's t-test, whereas beta-Actin control data were compared with the use of Mann-Whitney U test.
  
  
  RESULTS
  The average relative amount of RCAS1 was significantly lower in women with induced stillbirths than in women with induced labor at term. Similarly, significantly lower RCAS1 placental levels were observed in patients with spontaneous stillbirths than in women with spontaneous labor at term. Significant differences in RCAS1 expression were also observed with the respect to the beginning of the stillbirth: spontaneous and induced. Lowest RCAS1 placental levels were observed in women with spontaneous stillbirth.
  
  
  CONCLUSIONS
  These preliminary results indicate that the alterations of RCAS1 expression in the human placenta may be involved in the changes of maternal immune system that take place during stillbirth.
authors.affiliation: Department of Gynecology and Infertility, Jagiellonian University, 23 Kopernik Str, 31-501 Krakow, Poland. mowicher@cyf-kr.edu.pl
authors.forename: Lukasz
authors.initials: L
authors.lastname: Wicherek
authors.forename: Marek
authors.initials: M
authors.lastname: Klimek
authors.forename: Artur
authors.initials: A
authors.lastname: Czekierdowski
authors.forename: Tadeusz J
authors.initials: TJ
authors.lastname: Popiela
authors.forename: Krystyna
authors.initials: K
authors.lastname: Galazka
authors.forename: Tomasz
authors.initials: T
authors.lastname: Tetlak
authors.forename: Andrzej
authors.initials: A
authors.lastname: Gilowski
authors.forename: Magdalena
authors.initials: M
authors.lastname: Dutsch-Wicherek
mesh_terms: D000328:Adult; D000951:Antigens, Neoplasm / Q000378:metabolism*; D005260:Female; D006801:Humans; D008431:Maternal-Fetal Exchange; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D050497:Stillbirth / Q000453:epidemiology
chemical_list: D000951:Antigens, Neoplasm; C120762:EBAG9 protein, human