PubMed Health⌕ Search

Biomedical subjects

S C Riley

Publications and source records attributed to S C Riley.

At least 55 records · Page 3Linked to original sources
PubMed1995

Localization of neutral endopeptidase in the ovine uterus and conceptus during the oestrous cycle and early pregnancy.

Neutral endopeptidase (NEP; EC 3.4.24.11), an enzyme which metabolizes several peptides (including oxytocin and endothelins) implicated in the control of uterine function, was found to be localized in the ovine uterus throughout the oestrous cycle and in the uterus and conceptus during early pregnancy, using immunohistochemical techniques. Positive NEP immunoreactivity was found in the endometrium principally in stromal cells, in the vasculature in endothelial and vascular smooth muscle cells, and also weakly in some glandular epithelial cells. In a layer of stromal fibroblasts several cells in thickness underlying the luminal epithelium, staining was much weaker than that in the deeper stromal cells throughout the period examined. NEP staining was also present in smooth muscle cells of the myometrium at all times, and was most intense in the layer of cells adjacent to the endometrium. In the conceptus, NEP immunohistochemical staining was found in uninucleate cells, but not in binucleate trophoblast cells, in epithelial cells of the allantois and amnion, and in the heart and brain of the Day-20 embryo. In ovariectomized ewes treated with oestrogen or progesterone separately or remaining untreated, immunohistochemical staining of NEP was stronger when compared with intact ewes, in caruncular and intercaruncular stroma and epithelia, in glands, in the vasculature and in myometrium. The staining was less intense in all cell types in ewes receiving oestrogen plus progesterone. The expression of NEP and its specific regionalization within the uterus indicate a mechanism by which the availability of biologically important peptides involved in the regulation of the oestrous cycle and implantation, including oxytocin and endothelin, can be controlled by regulation of their metabolism.

Animals↗
PubMed1995

Immunolocalization of endothelin and neutral endopeptidase in the endometrium of users of subdermally implanted levonorgestrel (Norplant).

Subdermally implanted slow-release levonorgestrel (Norplant), a widely used effective contraceptive, has a high rate of discontinuation due to unacceptable menstrual bleeding disturbances. Endothelin (ET), a potent vasoconstrictor, varies across the menstrual cycle in normal endometrium. It has been proposed that ET has a potential paracrine role in the regulation of uterine blood flow. Neutral endopeptidase (NEP), a membrane-bound ecto-enzyme, can inactivate ET and is localized principally in endometrial stroma. We have compared the immuno-localization of ET and NEP in endometrial biopsies from Indonesian women using Norplant with normal controls. Differences were observed in the glandular and luminal epithelium of Norplant-treated subjects, where ET immunostaining was low while NEP immunoreactivity was increased. The latter may represent a local increase in enzyme activity, potentially explaining the reduced ET immunoreactivity. There was no correlation of ET immuno-reactivity with the duration of implant use or total number of bleeding days. The marked differences in the ET immunostaining pattern in Norplant users, with their increased risk of abnormal uterine bleeding, suggest that ET may be important in controlling menstrual bleeding. Whether endometrial epithelial cell ET has a role as a mitogen in endometrial repair and regeneration, or as a vasoconstrictor important in the cessation of bleeding following menstruation, remains to be determined.

Atrophy↗
PubMed1995

Tissue inhibitors of metalloproteinases in endometrium of ovariectomized steroid-treated ewes and during the estrous cycle and early pregnancy.

Tissue inhibitors of metalloproteinases (TIMPs) have an important role in remodeling of tissues and are likely to be implicated in uterine function, including embryo implantation and placentation. Expression of mRNA for TIMP-1 and TIMP-2 was examined by Northern analysis of endometrial RNA derived from steroid-treated ovariectomized ewes and from intact ewes during the estrous cycle and early pregnancy. Expression of mRNA for TIMP-1 (transcript size 0.9 kb), high in ovariectomized ewes, was substantially reduced by estrogen and to a lesser extent by progesterone. In cyclic and pregnant animals, abundance remained low until Day 10 and then increased, with high abundance continuing to Day 20 in the pregnant animals. Two transcripts for TIMP-2 were detected in ovine tissues--the 3.5-kb transcript and, in greater abundance, the 1.0-kb transcript. In ovariectomized ewes, endometrial abundance of both transcripts was low, and it decreased following estrogen treatment but was stimulated by progesterone alone or progesterone in the presence of estrogen. Abundance of TIMP-2 mRNA increased from Day 4 to Day 14 of the cycle. During early pregnancy, expression of the 1.0-kb transcript increased from Day 4 to Days 12-14 and was maintained at a high level to Day 20, whereas the 3.5-kb transcript decreased after Day 14 to very low levels by Day 20. In contrast with this pattern of regulated expression of TIMP, mRNA for proMMP-1 and for proMMP-3 was not detectable in any of the same tissues by Northern analysis. TIMP-1 protein was immunolocalized to both epithelium and stroma of intact endometrium, and the intensity of immunostaining was correlated with mRNA levels. TIMP-1 was secreted by both epithelial and stromal cells in primary culture, and its identity was confirmed by Western analysis, while reverse zymography demonstrated TIMP-1 and TIMP-2 along with a putative ovine TIMP-3 in the culture medium from both cell types. The precise role of TIMP in the endometrium remains to be established.

Animals↗
PubMed1995

Endothelin-1 and endothelin receptors are present in the sheep uterus and conceptus at implantation.

Previous studies have demonstrated that endothelin is present in the ovine endometrium and increases at around the expected time of implantation. To characterize further uterine endothelin at the time of establishment of pregnancy in sheep, endothelin was measured by radioimmunoassay in uterine flushings obtained during the oestrous cycle and in pregnant ewes up to the time of implantation (day 16). During the oestrous cycle, the highest amounts of endothelin were present in uterine flushings on day 14 (1.1 +/- 0.2 ng endothelin/uterus). During early pregnancy, basal levels of endothelin (0.5-0.6 ng endothelin/uterus) were present in uterine flushings for the first 10 days and then increased on day 14 to levels similar to those found at the equivalent stage of the oestrous cycle. On days 15 and 16 of pregnancy, endothelin content in the uterine lumen increased to significantly (P < 0.05) higher concentrations (2.9 +/- 0.4 ng endothelin/uterus) when compared with the non-fertile cycle. The principal isoform present in flushings at the time of implantation was endothelin-1, as determined by reverse-phase HPLC. Endothelin was released principally by purified endometrial epithelial cells in culture, with barely detectable amounts released by endometrial stromal cells or conceptus tissue, which is consistent with the epithelium being the principal source of endothelin in the uterine lumen. Endothelin binding sites were present in endometrium and myometrium, as demonstrated by specific binding of 125I-labelled endothelin-1, which was saturable and displaced by endothelin-1. Both endothelinA and B sub-types of receptors were present as demonstrated by the biphasic displacement of 125I-labelled endothelin-1 binding by the specific endothelinB agonist BQ3020. These were localised principally on luminal and glandular epithelium and in the vasculature of the endometrium and myometrium as shown by autoradiography. Endothelin receptors were also present on the conceptus obtained at the time of implantation. In the day 20 conceptus, endothelin immunostaining was localised principally in the heart, in trophoblast in uninucleate but not in binucleate cells, and in fetal membranes. This immunostaining of the conceptus may represent binding to receptor sites. It is concluded that endothelin-1 is present in the uterine lumen and may play an important role in the paracrine regulation of the conceptus and endometrium at the time of rapid embryo development, implantation and early placentation.

Animals↗
PubMed1994

Production and characterization of endothelin released by human endometrial epithelial cells in culture.

This study identified and characterized endothelin (ET) produced by human endometrial epithelial cells cultured under serum-free conditions, compared the ET released by cells derived from proliferative and secretory phase endometrium, and examined the regulation of ET released by these cells. ET messenger RNA was detected in normal human endometrium with maximal expression in the mid-late secretory phase. Immunoreactive ET released into culture media by separated endometrial epithelial and stromal cells was almost entirely of epithelial cell origin, consistent with the previous immunohistochemical findings. This was identified as ET-1 by reverse phase high-pressure liquid chromatography, and the fractionated conditioned media exhibited bioactivity similar to that of standard ET-1. Mean ET production was greater from cells derived from proliferative phase endometrium cultured either in serum (P < 0.02) or serum-free conditions (P < 0.02). Fetal calf serum stimulated ET-1 production from epithelial cells in a dose-responsive manner. ET production was also stimulated by transforming growth factor-beta 1 (2, 5 & 10 ng/mL) and IL-1 alpha (10 & 100 IU/mL) under serum-free conditions but always to a lesser extent than stimulation by serum. The production of ET in human endometrium underlines a potential role for ET in endometrial function.

Animals↗
PubMed1994

Endothelin in the ovine uterus during the oestrous cycle and early pregnancy.

Endothelin, which has potent vasoconstrictor and mitogenic actions, was measured by radioimmunoassay in tissue extracts of sheep endometrium and myometrium and was found to be present in similar amounts in both tissues during the oestrous cycle and in increasing amounts during the first 20 days of pregnancy (250-630 pg g-1 wet weight). Immunoreactive endothelin extracted from endometrium eluted at the same position as standard endothelin-1 on reverse-phase HPLC. Immunohistochemical techniques demonstrated that during the oestrous cycle endothelin immunoreactivity was very low in caruncular and intercaruncular stroma, luminal epithelium, outer and inner glandular epithelium, myometrium and blood vessels until after day 12 (oestrus: day 0). Staining increased in all but the inner glands to day 16 and the most intense staining was found in intercaruncular luminal epithelium and outer glands and in myometrium, although endothelin in tissue extracts did not change over this period. During early pregnancy (days 4-20), staining in intercaruncular areas and in myometrium increased slightly from day 4 to day 12 to a maximum which was maintained from day 15 to day 20. Intensity of staining in caruncles increased only from day 15, particularly in the epithelium. Immunoreactive endothelin was also present in the trophoblast cells of the embryo on day 20 of pregnancy. Strong endothelin immunostaining was observed in uteri from ovariectomized ewes, particularly in epithelial cells and in blood vessels. The intensity of immunostaining in epithelium and epithelial cells and in blood vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Foetal endocrine maturation.

In domestic ruminants such as the sheep, birth is effected through sequential maturation of the foetal hypothalamic-pituitary-adrenal (HPA) axis, leading to the increased output of cortisol. Factors regulating foetal pituitary adrenocorticotrophin (ACTH) secretion have been delineated, and these include corticotrophin releasing hormone (CRH), arginine vasopressin, prostaglandin (PG) E2 and endogenous opioids. The pre-partum increase in foetal plasma ACTH is associated with a rise in pro-opiomelanocortin (POMC) mRNA in the foetal pars distalis, and with an altered pattern of POMC post-translational processing. Foetal adrenal activation results from an increase in ACTH receptors and enhanced coupling through the Gs protein to adenylate cyclase, and increased expression of key steroidogenic enzymes including P450c17. Cortisol modulates the mechanism by which ACTH activates foetal adrenal function, through specific glucocorticoid receptors (GR) in the foetal adrenal cortex. Although the numbers of GR change with gestation, the relative abundance of GR mRNA does not, pointing to post-translational regulatory mechanisms. Cortisol also stimulates an increase in the concentration of its own high affinity binding protein (corticosteroid binding globulin; CBG) in the foetal circulation, apparently by increasing CBG gene expression in the foetal liver, and by altering the extent of foetal CBG glycosylation in a manner that would be expected to decrease the metabolic clearance of this glycoprotein. Clear evidence for placental CRH and ACTH production is lacking in sheep, but PGE2, produced in increasing amounts by the placenta during late pregnancy, may augment the drive to HPA maturation. Aspects of the maturational pathway of cortisol biosynthesis have been described in other species, including the horse, and some comparison is made with the more detailed information currently available from species such as the sheep.

Animals↗
PubMed1993

Changes in the abundance of mRNA for type-I 3 beta-hydroxysteroid dehydrogenase/delta 5-->delta 4 isomerase in the human placenta and fetal membranes during pregnancy and labor.

A local decrease in progesterone synthesis in the placenta and fetal membranes has long been proposed as a possible mechanism in the control of human labor. We have examined whether changes occur in the abundance of mRNA for 3 beta-hydroxysteroid dehydrogenase/delta 5-->delta 4 isomerase (3 beta-HSD), the enzyme which catalyzes the conversion of pregnenolone to progesterone in human placenta and fetal membranes, by Northern blot analysis using a cDNA probe to human placental type-I 3 beta-HSD, the predominant isoenzyme in the placenta. The abundance of 3 beta-HSD mRNA (1.7-kb transcript) was about 10-fold greater in term placenta than in chorio-decidua, but undetectable in total RNA from amnion. There was no change in the abundance of 3 beta-HSD mRNA in either placenta or chorio-decidua obtained after elective cesarean section at term, after preterm labor, or after term or postterm vaginal delivery. We conclude that the abundance of 3 beta-HSD mRNA does not change in the placenta or fetal membranes with labor, consistent with the view that changes in 3 beta-HSD gene expression and decreased progesterone production are unlikely to effect intrauterine paracrine/autocrine regulatory mechanisms leading to term or preterm labor in women.

Blotting, Northern↗
PubMed1992

Dexamethasone inhibits basal and stimulated prostaglandin E2 output from human placental cells by inhibition of prostaglandin H synthase.

In view of the temporal relation between elevated concentrations of glucocorticoids and prostaglandins (PG) at the time of parturition, we have examined the effects of dexamethasone on PGE2 output by mixed cell preparations from human placentae at term maintained in short-term (48 or 96 h) culture. Dexamethasone inhibited placental PGE2 output in a dose-dependent fashion. The effect on placental cells was more marked than on short-term cultures of amnion cells and was not influenced by the presence of progesterone. Dexamethasone also inhibited stimulated PGE2 output after addition of arachidonic acid. These results suggest that glucocorticoids inhibit placental PG output by a mechanism involving attenuation of PG synthase activity or expression and do not support a direct causal role for elevated maternal or fetal glucocorticoids at term on increased placental PG biosynthesis.

Arachidonic Acid↗
PubMed1992

Localization of 15-hydroxy prostaglandin dehydrogenase in human fetal membranes, decidua, and placenta during pregnancy.

Localization of NAD(+)-dependent 15-hydroxy prostaglandin dehydrogenase (type I-PGDH) may influence local concentrations of bioactive eicosanoids within intrauterine tissues. In early pregnancy (6-9 weeks), IR-PGDH was localized by immunohistochemistry to syncytiotrophoblast, cytotrophoblast, and intermediate trophoblast of placenta. At 23-30 weeks of gestation and at term IR-PGDH was present in syncytiotrophoblast and intermediate trophoblast, but not in cytotrophoblast in placenta. It was absent from amnion, and distributed within the trophoblast cell layer of extraplacental chorion variably at 23-30 weeks, but consistently at term. We speculate that PGDH is ideally localized to metabolize and to maintain low concentrations of primary prostaglandins in the fetal membranes for much of gestation.

Decidua↗
PubMed1992

Localization of the growth hormone receptor, identified by immunocytochemistry, in second trimester human fetal tissues and in placenta throughout gestation.

Pituitary GH secretion appears largely unnecessary for the attainment of normal birth size in many species, including man. This is believed to be due to an immaturity and/or an absence of GH receptors in many fetal tissues. However, in vitro studies using late first trimester human fetal tissues have demonstrated mitogenic actions of GH on liver and stimulation of insulin biosynthesis in pancreas. To resolve this discrepancy, we have employed immunocytochemistry to identify the presence and distribution of GH receptors in various human fetal tissues. Fetuses of 14-16 weeks gestation were obtained after therapeutic abortion, tissues were fixed, and immunocytochemistry was performed using monoclonal antibodies against purified rat or rabbit GH receptor. The specificity of staining was confirmed by preabsorption of the antibodies with 1) adult rat liver membranes or 2) human fetal liver membranes, both of which possess specific GH-binding sites, or 3) human fetal skeletal muscle membranes, which do not specifically bind GH. Positive staining was seen in a subpopulation of liver parenchymal cells, in the ductal and endocrine tissue of pancreas, in the germinal layer of the epidermis and the deeper dermal layers of skin, and in the tubular epithelium of kidney. No immunopositive staining was seen in skeletal or cardiac muscle, epiphyseal growth plate, lung, intestine, or adrenal. Positive staining was present in the neuronal cell bodies of the cerebral cortex. GH receptor was also detectable as early as 8 weeks gestation in syncytial layers of the placenta and was maintained until term. Results demonstrate the presence of immunoreactive GH receptor/binding protein in some human fetal tissues early in development. In particular, these results would support a role for GH in the growth and function of liver and pancreas.

Extraembryonic Membranes↗
PubMed1992

Immunohistochemical localization of 3 beta-hydroxy-5-ene-steroid dehydrogenase/delta 5----delta 4 isomerase in human placenta and fetal membranes throughout gestation.

The regulation of steroid production by the placenta and fetal membranes is important for both the maintenance of pregnancy and the timing of parturition. 3 beta-Hydroxy-5-ene-steroid dehydrogenase/delta 5----delta 4-isomerase (3 beta HSD) catalyzes an obligatory step in the biosynthesis of steroid hormones. We have determined the localization of 3 beta HSD in the human placenta, fetal membranes, and umbilical cord throughout gestation by immunohistochemical analysis, using a polyclonal antibody raised in rabbits against a purified preparation of human placental 3 beta HSD. In placenta, immunoreactive (IR-) 3 beta HSD was localized in the syncytiotrophoblast and intermediate trophoblast cells at both villous and extravillous sites, but not in cytotrophoblast cells from 6 weeks gestation to term. At 6-7 weeks gestation, IR-3 beta HSD was distributed in the cytoplasm of syncytiotrophoblast in about half of placental villi. By 12-14 weeks, the syncytiotrophoblast of all placental villi stained positively for 3 beta HSD. In the fetal membranes, strong IR-3 beta HSD staining was found in the trophoblast and reticular layers of chorion and in invasive trophoblast cells in decidua, and weakly in decidual stromal cells and amniotic epithelium. No IR-3 beta HSD was found in amnion on the placental plate, but in the umbilical cord, IR-3 beta HSD was present in the amniotic epithelium and also in fibroblast cells in Warton's jelly. These observations demonstrate that the localization of 3 beta HSD immunoreactivity and, therefore, the presumed sites of delta 5- to delta 4-steroid interconversion throughout gestation are principally the syncytiotrophoblast and intermediate trophoblast cells in placenta and the trophoblast cells in chorion and decidua in fetal membranes.

Extraembryonic Membranes↗
PubMed1992

Immunohistochemical localization of 3 beta-hydroxysteroid/delta 5-delta 4-isomerase, tyrosine hydroxylase and phenylethanolamine N-methyl transferase in adrenal glands of sheep fetuses throughout gestation and in neonates.

Immunoreactive 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase (3 beta-HSD) was localized in adrenal glands of sheep fetuses in cortical-type cells, but not in medullary-type cells, from day 43 of gestation to term and in 2-4-day-old neonates. From day 54 of gestation, the formation of distinct zones within the adrenal cortex was apparent and immunoreactive 3 beta-HSD was found in cortical cells in the zona fasciculata and in groups and cords of cortical cells within the developing medulla, with weak positive staining in the zona glomerulosa. At this stage, most medullary cells were positive for immunoreactive tyrosine hydroxylase, and some of these cells with a juxtacortical distribution also stained positively for immunoreactive phenylethanolamine N-methyl transferase (PNMT). Between days 65 and 130, the adrenal medulla increased in size with little change in the width of the cortex. Organization and zonation of immunoreactive 3 beta-HSD staining cells were evident in the zona fasciculata and in groups of cells in the medulla. Between day 130 and term, uniform immunoreactive 3 beta-HSD staining was found throughout the zona fasciculata, and there was also staining in single cells and small clusters of cells throughout the medulla. At this stage, immunoreactive tyrosine hydroxylase was distributed in most cells throughout the medulla, but in two distinct patterns: cells staining intensely for immunoreactive tyrosine hydroxylase in the central region of the medulla, and cells exhibiting weaker staining for immunoreactive tyrosine hydroxylase localized in a juxta-cortical position. These juxta-cortical cells were also positive for immunoreactive PNMT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1991

Immunohistochemical localization of prostaglandin H synthase in the sheep placenta from early pregnancy to term.

Prostaglandin H synthase (PGHS) activity within intrauterine tissues is considered to catalyze a critical step in prostaglandin (PG) biosynthesis at parturition. In sheep, the placenta is a major site of PG production throughout pregnancy, but little information is available concerning the cells that are responsible. Therefore we determined the distribution of immunoreactive (IR-) PGHS in ovine placental tissue obtained at different times of pregnancy using immunohistochemical techniques. In placentomes from early pregnancy (Days 30-54), IR-PGHS was present in maternal epithelial syncytium, but was not detectable in trophoblast cells. Between Day 54 and Day 100, the number of cells that stained positive for PGHS declined in the maternal epithelial layer in the body of the placenta, but IR-PGHS was present in maternal epithelial cells overlying the vascular cones of the placental hemophagous zone. It was also present in the chorionic fibroblasts, but remained undetectable from all classes of trophoblast cells. IR-PGHS was first detectable in the trophoblastic epithelium by Day 114. Between Day 119 and term the trophoblast mononuclear epithelial cells were intensely immunopositive for PGHS, although immunonegative binucleate cells were present. The maternal epithelium was immunonegative except during the last 7-10 days of pregnancy when PGHS immunostaining appeared in both basal and apical regions of the placenta. Thus, the cellular localization of IR-PGHS changes during ovine pregnancy, from predominantly maternal during the first half of gestation to undetectable and then to predominantly trophoblastic between Day 114 and term, suggesting a gestation-dependent change in sites of PG production during ovine pregnancy. Appearance of IR-PGHS in the trophoblast precedes activation of the fetal hypothalamic-pituitary-adrenal axis, generally considered to provide the trigger to the onset of parturition in sheep, and would therefore appear to be regulated through alternative pathways or mechanisms.

Animals↗
PubMed1991

The localization and distribution of corticotropin-releasing hormone in the human placenta and fetal membranes throughout gestation.

Using immunohistochemical techniques, we have determined the localization and distribution of CRH immunoreactivity (CRH-IR) in the human placenta, fetal membranes, decidua, and umbilical cord. Tissues were obtained at 6-8 weeks of pregnancy, at term, in association with premature birth, and from patients with pregnancy-induced hypertension or diabetes mellitus. A polyclonal antibody to the epithelial cell marker cytokeratin was used to identify trophoblast cells. CRH-IR was not detected in placenta or decidua at 6-8 weeks gestation. In tissues obtained after idiopathic premature delivery after 21 weeks gestation, positive CRH staining was found in placenta in syncytiotrophoblast and intermediate trophoblast, but not cytotrophoblast. CRH-IR was present in intermediate trophoblast cells that had invaded maternal blood vessels in decidua basalis. In the fetal membranes, CRH-IR was localized in the epithelium and subepithelial cells of amnion, in the trophoblast layer, in some cells of the reticular and cellular layers of chorion, and in some stromal cells and invasive trophoblast cells of decidua. CRH-IR was found in the amniotic epithelium of the umbilical cord and in the musculature of the umbilical vessels. This pattern of distribution of CRH-IR was found in tissues from 21 weeks gestation to term and postterm, and was similar in tissues examined from patients with pregnancy-induced hypertension and diabetes mellitus. These results show clearly that in placenta and membranes, CRH is localized primarily to syncytiotrophoblast and intermediate trophoblast, but not to cytotrophoblast cells. We suggest that the localization of CRH-IR is consistent with CRH affecting paracrine/autocrine interactions within the placenta, fetal membranes, and decidua that may be involved in the maturation of the fetal hypothalamic-pituitary-adrenal axis and in the stimulus and maintainance of labor.

Amnion↗
PubMed1990

Immunocytochemical distribution and localization of 15-hydroxyprostaglandin dehydrogenase in human fetal membranes, decidua, and placenta.

Biochemical studies have shown the presence of type I oxidized nicotinamide-adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase in human fetal membranes, decidua, and placenta. However, the localization of prostaglandin dehydrogenase within these tissues is not known. Because the distribution of prostaglandin dehydrogenase may affect the concentration of prostaglandins that reach the myometrium, we used immunocytochemistry to localize immunoreactive prostaglandin dehydrogenase in fetal membranes and placenta. We also examined whether this distribution changed with labor. Tissues were collected at term elective cesarean section or after term spontaneous labor and delivery, were fixed, embeded, and sectioned at 5 microns. Immunoreactive prostaglandin dehydrogenase was determined with a polyclonal primary antibody to human placental prostaglandin dehydrogenase and visualized with the avidin-biotin procedure. Epithelial and epithelium-derived cells were identified by positive staining with a polyclonal antikeratin primary antibody. Cytokeratin staining was observed in amniotic epithelium, trophoblast layer of chorion, invading trophoblast in decidua, and all subsets of trophoblast in the placenta. Immunoreactive prostaglandin dehydrogenase was localized to the trophoblast layer of chorion, invading trophoblast in decidua, and in syncytiotrophoblast and intermediate trophoblast but not cytotrophoblast in the placenta. In chorion, approximately 50% to 60% of the nonvacuolated trophoblast cells stained positively for prostaglandin dehydrogenase. There was no change in the localization of immunoreactive prostaglandin dehydrogenase in any tissue in association with labor.

Amnion↗
PubMed1990

Is the inhibitory effect of progesterone on endometrial prostaglandin F2 alpha production due to an inhibition of protein synthesis?

Progesterone and a high concentration of oestradiol (i) reduced the outputs of prostaglandin (PG) F2 alpha and, to a lesser extent, PGE2 from Day-7 and Day-15 guinea-pig endometrium in culture, but had little or no effect on the output of 6-keto-PGF1 alpha, (ii) prevented the increase in PGH synthase concentrations which normally occur in Day-7 and Day-15 guinea-pig endometrium during culture, and (iii) reduced the synthesis of secreted proteins by Day-15 guinea-pig endometrium in culture. These findings suggest that the inhibitory effect of progesterone and of high concentrations of oestradiol on endometrium PGF2 alpha synthesis is due to an inhibition of the syntheses of proteins involved in PGF2 alpha production.

6-Ketoprostaglandin F1 alpha↗