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. RCASI participates in the inhibition of maternal immune response during pregnancy. The alterations of RCASI 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 RCASI expression in placentas obtained following stillbirths or normal term births. Methods: RCASI expression was evaluated by Western blot method with the use of monoclonal anti-RCASI 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 RCASI 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 RCASI was significantly lower in women with induced stillbirths than in women with induced labor at term. Similarly, significantly lower RCASI placental levels were observed in patients with spontaneous stillbirths than in women with spontaneous labor at term. Significant differences in RCASI expression were also observed with the respect to the beginning of the stillbirth: spontaneous and induced. Lowest RCASI placental levels were observed in women with spontaneous stillbirth. Conclusions: These preliminary results indicate that the alterations of RCASI expression in the human placenta may be involved in the changes of maternal immune system that take place during stillbirth. © 2005 Wicherek et al; licensee BioMed Central Ltd.
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CITATION STYLE
Wicherek, L., Klimek, M., Czekierdowski, A., Popiela, T. J., Galazka, K., Tetlak, T., … Dutsch-Wicherek, M. (2005). The placental RCAS1 expression during stillbirth. Reproductive Biology and Endocrinology, 3. https://doi.org/10.1186/1477-7827-3-24
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