“…Recently, elevated concentrations of a stable PGF 2 α metabolite (PGFM) were found in the feces of several felid species in the last trimester of pregnancy [14]. In the present study, the PGFM level, measured in feline plasma blood collected just before ovariohysterectomy, was low during the first and second trimesters of pregnancy and then started to increase for the last 3 weeks of gestation.…”
Section: Discussionsupporting
confidence: 45%
“…Recently, the PGF 2 α inactive metabolite 13,14-dihydro-15-keto prostaglandin F 2 α (PGFM), measured in the feces, was shown to be a precise pregnancy indicator in several felid species, including the domestic cat, during the last trimester of gestation [14]. The uteroplacental complex was proposed to be a source of PGF 2 α in cats [14].…”
Section: Introductionmentioning
confidence: 99%
“…The uteroplacental complex was proposed to be a source of PGF 2 α in cats [14]. We hypothesize that the placenta of the domestic cat synthesizes PGF 2 α in a time-dependent manner.…”
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 (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 PGF2α and plasma PGFM were elevated towards the end of pregnancy (P < 0.001) 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.
“…Recently, elevated concentrations of a stable PGF 2 α metabolite (PGFM) were found in the feces of several felid species in the last trimester of pregnancy [14]. In the present study, the PGFM level, measured in feline plasma blood collected just before ovariohysterectomy, was low during the first and second trimesters of pregnancy and then started to increase for the last 3 weeks of gestation.…”
Section: Discussionsupporting
confidence: 45%
“…Recently, the PGF 2 α inactive metabolite 13,14-dihydro-15-keto prostaglandin F 2 α (PGFM), measured in the feces, was shown to be a precise pregnancy indicator in several felid species, including the domestic cat, during the last trimester of gestation [14]. The uteroplacental complex was proposed to be a source of PGF 2 α in cats [14].…”
Section: Introductionmentioning
confidence: 99%
“…The uteroplacental complex was proposed to be a source of PGF 2 α in cats [14]. We hypothesize that the placenta of the domestic cat synthesizes PGF 2 α in a time-dependent manner.…”
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 (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 PGF2α and plasma PGFM were elevated towards the end of pregnancy (P < 0.001) 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.
“…A similar luteolytic trend was shown in domestic cats, in which elevated concentrations of PGF2a could be detected in the placenta and its metabolite in blood serum during the preparturition period [67]; this suggests a luteolytic action of PGF2a at this time point. During pseudopregnancy, however, this placental signal is missing, and PGFM elevations are not evident at any time during the nonpregnant luteal phase of domestic cats and other feline species [65,68]. Thus, a passive luteolysis in pseudopregnancy might be considered, although the role of luteotropic and luteolytic factors, and in particular of PGF2a, must be investigated further.…”
Contents
The corpus luteum (CL) is a transient hormone gland on the ovary that produces progesterone (P4) for the maintenance of pregnancy. It develops from residual follicular granulosa and theca cells after ovulation. Very little is known about the cellular and hormonal processes within CLs obtained from pregnant and pseudopregnant felids. Therefore, our aim was to review the luteal function in feline CLs of different reproductive stages in conjunction with our data obtained in domestic cats and Eurasian lynxes. Corpus luteum function in lynxes is of particular interest, as a post‐partum luteal activity was suggested based on repeated ultrasonography and endocrine examinations. Histology of CL from pregnant and pseudopregnant domestic cats clearly reflects the luteal function. The formation of the CL after ovulation is characterized by transforming of theca and granulosa cells into steroidogenic luteal cells and is accompanied by increased intraluteal and circulating P4 levels. Luteal regression is steadily progressive; the first signs (coarsed vacuolization, increased proportion of non‐steroidogenic cells) are visible already in CL from the second trimester of pregnancy.
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