Prostaglandin synthesis enzymes' gene transcription in bitches with endometritis

Contents Endometritis is a major cause of infertility in many domestic species. However, until now the pathogenesis of the endometritis in the bitch is unclear. The aim of this study was to evaluate the gene transcription pattern of prostaglandin (PG) synthesis enzymes (cyclooxygenase [COX2], PTGES‐...

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Published inReproduction in domestic animals Vol. 52; no. S2; pp. 298 - 302
Main Authors García Mitacek, MC, Praderio, RG, Stornelli, MC, Sota, RL, Stornelli, MA
Format Journal Article
LanguageEnglish
Published Germany Blackwell Publishing Ltd 01.04.2017
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Summary:Contents Endometritis is a major cause of infertility in many domestic species. However, until now the pathogenesis of the endometritis in the bitch is unclear. The aim of this study was to evaluate the gene transcription pattern of prostaglandin (PG) synthesis enzymes (cyclooxygenase [COX2], PTGES‐1 and PGFS) in the endometrium of bitches with or without endometritis. Thirty mixed breed bitches in dioestrus, aged between 1 and 5 years, and weighing between 10 and 30 kg were used. After ovariohysterectomy (OVX), uterine biopsy samples were collected from the middle part of both horns. Then, endometrial epithelium was collected using the cytobrush method and mRNA analysis was performed by real‐time RT‐PCR. Data were analysed with Kruskal–Wallis anova using the sas® software. Uterine condition was identified by endometrial biopsies (normal endometria [n = 11; NE], acute endometritis [n = 10; AE] and chronic endometritis [n = 9; CE]). The COX2, PTGES‐1 and PGFS/AKR1C3 mRNA expression in bitches with and without endometritis was similar. Except for PGFS/AKR1C3, gene transcription of COX2 and PTGES‐1 was significantly increased in AE compared with CE. In addition, COX2 gene transcription was significantly increased in AE compared with NE. In contrast, no differences were found for COX2, PTGES‐1 and PGFS/AKR1C3 mRNA expression in the samples of NE compared with CE.
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ISSN:0936-6768
1439-0531
DOI:10.1111/rda.12950