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Placental Origin of Prostaglandin F(2α) in the Domestic Cat

In the present study, the question was addressed whether the feline placenta can synthesize prostaglandin F(2α) (PGF(2α)). 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 upr...

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Detalles Bibliográficos
Autores principales: Siemieniuch, Marta J., Jursza, Ewelina, Szóstek, Anna Z., Zschockelt, Lina, Boos, Alois, Kowalewski, Mariusz P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934528/
https://www.ncbi.nlm.nih.gov/pubmed/24659861
http://dx.doi.org/10.1155/2014/364787
Descripción
Sumario:In the present study, the question was addressed whether the feline placenta can synthesize prostaglandin F(2α) (PGF(2α)). 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 PGF(2α) and plasma PGFM were elevated towards the end of pregnancy (P < 0.001) compared with earlier weeks of pregnancy. The content of PGF(2α) 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 PGF(2α) levels in placental tissue concomitant with an upregulation of placental PTGS2.