Placental Origin of Prostaglandin F2α in the Domestic Cat. (10th February 2014)

• Record Type: Journal Article
• Authors: Siemieniuch, Marta J.; Jursza, Ewelina; Szóstek, Anna Z.; Zschockelt, Lina; Boos, Alois; Kowalewski, Mariusz P.
• Other Names: Galvão António Miguel Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2014(2014)
• Publication Date: 2014-02-10
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2014/364787
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : In the present study, the question was addressed whether the feline placenta can synthesize prostaglandin F2 α (PGF2 α ). The PGFS protein was elevated, particularly at 2.5–3 weeks of pregnancy compared to 7-8 (P < 0.05 ) and 8.5–9 weeks (P < 0.001 ). Transcripts for PGFS were significantly upregulated at 2.5–3 weeks of pregnancy and then gradually declined towards the end of gestation (P < 0.001 ). Transcripts for PTGS2 were only upregulated in placentas from queens close to term (P < 0.001 ) 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 PGF2 α and plasma PGFM were elevated towards the end of pregnancy (P < 0.001 ) compared with earlier weeks of pregnancy. The content of PGF2 α 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 PGF2 α levels in placental tissue concomitant with an upregulation of placental PTGS2.