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Mediators of Inflammation
Volume 2014, Article ID 364787, 8 pages
Research Article

Placental Origin of Prostaglandin F2α in the Domestic Cat

1Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, Tuwima Street, Olsztyn 10-748, Poland
2Leibniz Institute for Zoo and Wildlife Research, Alfred-Kowalke Straße 17, 10315 Berlin, Germany
3Institute of Veterinary Anatomy, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 260, 8057 Zurich, Switzerland

Received 18 November 2013; Accepted 22 December 2013; Published 11 February 2014

Academic Editor: António Miguel Galvão

Copyright © 2014 Marta J. Siemieniuch et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In the present study, the question was addressed whether the feline placenta can synthesize prostaglandin F2α (PGF2α). The PGFS protein was elevated, particularly at 2.5–3 weeks of pregnancy compared to 7-8 ( ) and 8.5–9 weeks ( ). Transcripts for PGFS were significantly upregulated at 2.5–3 weeks of pregnancy and then gradually declined towards the end of gestation ( ). Transcripts for PTGS2 were only upregulated in placentas from queens close to term ( ) compared with earlier phases. Staining of PTGS2 showed distinct positive signals in placentas obtained during the last week before labor, particularly in the strongly invading trophoblast surrounding blood vessels, and also in decidual cells. Shortly after implantation, signals for PGFS were localized in the trophoblast cells. Near term, PGFS staining was seen mainly in decidual cells. Both placental PGF2α and plasma PGFM were elevated towards the end of pregnancy ( ) compared with earlier weeks of pregnancy. The content of PGF2α in extracted placenta mirrored the PGFM level in plasma of pregnant females. During late gestation there is a significant increase in PGFM levels in maternal blood and of PGF2α levels in placental tissue concomitant with an upregulation of placental PTGS2.