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The aim of this study was to examine the effect of long-term treatment with glucocorticoids on the uterine response to oestradiol. Ovariectomized rats were treated with crystal triamcinolone acetonide (0.1 mg/100 g, i.m.) or saline (0.1 ml/100 g i.m.) for 29 days. Over this period five injections were administered, one per week. On the second day after the last triamcinolone injection, rats were treated with a single injection of oestradiol dipropionate (5 micrograms/100 g, s.c.) or vehicle (olive oil, 0.1 ml/100 g, s.c.). The effects of oestradiol in the uterus were determined by measuring mitotic index, bromodeoxyuridine (BrdU)-labelling index (BrdU was injected 2 h before the rats were killed; 2 mg/100 g, i.p.), and proliferating cell nuclear antigen (PCNA)-labelling index 24, 36 and 48 h after the injection of oestradiol or vehicle. Long-term treatment with glucocorticoids resulted in dissimilar changes in oestradiol-induced proliferation in epithelial and connective-tissue (stroma) components of the uterus. In luminal and glandular epithelia, there was an initial reduction in proliferation at 24 h, followed by an increase at 36 h and a further reduction at 48 h after the oestradiol injection. In stromal cells of the endometrium, triamcinolone treatment caused a large constant increase in oestradiol-induced proliferation throughout the experiment. The glucocorticoid treatment had no effect on the parameters without oestradiol administration.
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The present study was designed to determine the effect of the spatial gradient from the cervix to the uterine fundus on the control of local prostaglandin H synthase (PGHS) 2 mRNA expression. We performed total cesarean hysterectomies during the last trimester in 12 pregnant baboons, 7 not in labor and 5 in labor, and examined PGHS2 mRNA expression throughout the uterus. PGHS2 mRNA abundance was quantified by in situ hybridization and northern blot analysis in the uterine fundus, lower uterine segment and the different segments of the cervix. Quantitative northern blot and in situ analysis demonstrated a gradient of PGHS2 mRNA expression, with the highest levels at the level of the lower portion of the cervix and decreased expression through the mid- and upper portion of the cervix and lower uterine segment; the lowest levels of expression were seen in the uterine fundus. Moreover, cellular localization of PGHS2 mRNA and protein demonstrated high levels of expression in the cervical glandular epithelial cells with only occasional staining of smooth muscle cells in pregnant baboons. Decreased PGHS2 mRNA concentration gradient from the cervical external os to the fundus suggests that prostaglandin (PG) production in the uterus and cervix strongly depends on anatomical relations. This increased local PG production activity may be critical to pregnancy-associated lower uterine segment elongation, cervical softening and effacement in primate labor. These data provide a compelling biological basis for the use of PGHS2 inhibitors in the prophylaxis of preterm birth and cervical incompetence.
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The responsiveness of the uterus of the guinea-pig to oestrogen treatment was studied in the fetal and perinatal periods. Twenty-four hours after one dose of 1 mg oestradiol/kg body wt to the pregnant guinea-pig, there was no significant increase in uterine wet weight of the fetus but a sevenfold increase in the concentration of progesterone receptors. In the perinatal period, doses of 1,10 and 100 μg oestradiol led to as much as an 80% increase in uterine wet weight after 24 h in both 2- and 7-day-old guinea-pigs. On the other hand, levels of progesterone receptors in newborn animals showed a smaller increase (twofold) than that which occurred in the fetal uterus. In both fetal and newborn guinea-pigs, total oestradiol-receptor concentrations (both available and occupied binding sites) decreased significantly after treatment with oestradiol. It was concluded that the hormonal effect of oestradiol on progesterone-receptor synthesis can be expressed in the fetus and to an even greater extent than in the perinatal period over the same period of time. In the fetus, this response can be distinguished from the overall uterotrophic effect of oestradiol.
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This work was aimed at testing whether oestrogen-induced changes in the uterus are responsible for uterine eosinophil migration or whether the effect is due to a direct action of oestrogen on the eosinophils themselves. Uterine eosinophil migration in response to intraluminal administration of oestradiol-17β into one uterine horn was measured in the injected and in the untreated contralateral horns. Uterine genomic responses (luminal epithelial and myometrial hypertrophy and nucleolar enlargement), known to depend on the local intra-uterine oestrogen level, were measured to control for the absence of hormone recirculation to the uninjected horn. The effects of intravenously administered oestradiol were also determined. Intraluminal injection of 0·1 ng oestradiol had no effect on either horn. With 10 ng, only the injected horn exhibited the genomic responses while eosinophilia developed to the same extent in both horns. With 100 ng, the genomic responses and eosinophilia were identical in injected and in contralateral horns. The results show that eosinophil migration depends on systemic levels of oestrogen, thus indicating that it is due to an oestrogen-induced change in a property of eosinophil leukocytes rather than a change in the uterus itself. As water imbibition showed the same pattern of responses as eosinophilia, this lends further support to the hypothesis of a role for eosinophils in oestrogen-induced uterine oedema.
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SUMMARY
Loss of uptake during 24 hr. after administration of [3H]oestradiol showed approximately linear relationships between log uptake and time for uterus and vagina but not for skeletal muscle; these relationships were similar for mice pretreated with oestradiol. Uptake by uterus and vagina was less by about 50% when [3H]oestradiol was given to mice whose uteri and vaginae had reached maximum weight after pretreatment with oestradiol but cessation of growth of these organs was apparently not due to failure of their ability to take up oestradiol.
The relationship of uptake levels maintained in the uterus and vagina during 3 days and their consequent growth rate was studied.
When a second dose of [3H]oestradiol was given at various times after the first, new uptake, measured 1 hr. later, by uterus and vagina (but not skeletal muscle) was greatest when uptake remaining from the first dose was also greatest.
When a single dose of [3H]oestradiol (0·0039–2·5 μg.) was given to previously untreated mice or to mice with considerable oestradiol-induced uterine and vaginal growth, the only indications of any reduction of normal uptake ability were for the uterus when uptake was measured 1 hr. after doses greater than 0·11 μg.
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The importance of the nerve supply to the uterus for the functional activity of this organ is coming under increasing scrutiny (see Anderson, Bowerman & Melampy, 1963). In the present work the effect of interruption of nerves supplying the uterus upon implantation and the occurrence of pregnancy in the guinea-pig has been studied and the effects of section of the hypogastric and pelvic nerves compared.
Interruption of the nerve supply to the uterus was brought about by section of the hypogastric and/or pelvic nerves. The nerves were approached through a mid-ventral abdominal incision under pentobarbitone anaesthesia (supplemented when necessary with ether). With the aid of a dissecting microscope, about 1 cm. of each hypogastric nerve was removed medial to the ureters and just anterior to the aortic bifurcation; the pelvic nerves were exposed on both sides in the sacral region, lateral to the vagina and rectum, and sectioned as they
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SUMMARY
Priming of ovariectomized mice with 0·1 μg. oestradiol-17β for 3 days modified the subsequent cellular response of the uterus to oestrogen and progesterone. A single dose of oestradiol-17β (0·02 μg.), or progesterone (1 mg.), or of both hormones given simultaneously, stimulated mitosis in the epithelial cells of the endometrium (although not in the stromal cells). However, the same hormones administered to primed mice stimulated considerable stromal cell division and reduced epithelial mitosis. The maximal effect was found when both hormones were given on the 4th day after the end of priming. It is suggested that the priming of the uterus by oestrogen secreted by the ovary before mating is concerned in the abrupt change from epithelial to stromal cell division that occurs between days 3 and 4 of pregnancy, and is of importance in the sensitization of the uterus for implantation.
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ABSTRACT
Previous studies have shown that progesterone rapidly inhibits retention of uterine nuclear oestrogen receptor in several mammalian species. This effect of progesterone may constitute a general mechanism by which progesterone modulates oestrogen action. The objective of the present study was to examine the temporal pattern of progesterone inhibition of retention of occupied nuclear oestrogen receptors in the rat uterus at various sustained serum concentrations of progesterone. Silicone elastomer implants (1 cm) packed with crystalline oestrogen were placed s.c. in the flank region of ovariectomized adult rats. Twenty-four hours after placement of the implants, animals were either injected s.c. with 5 mg progesterone in corn oil every 24 h, treated with 2 × 5 cm implants of progesterone, or treated with 1 × 5 cm silicone elastomer implants of progesterone. Serum concentrations of progesterone at the time of necropsy were 0·47 ± 0·02, 0·18 ± 0·02 and 0·10 ± 0·01 μmol/l respectively. Control animals were given oestrogen implants alone and had a serum progesterone level of 0·03 ± 0·01 μmol/l. Occupied nuclear oestrogen receptor and cytosolic oestrogen and progesterone receptor levels (pmol/uterus) were measured between 0 and 48 h following progesterone treatment. Cytosolic progesterone receptor levels were suppressed similarly in all progesterone-treated groups compared with controls given oestrogen alone throughout the 48-h test period. Cytosolic oestrogen receptor levels were significantly suppressed at 12 h following progesterone treatment in all groups. Except for the highest (pharmacological) serum progesterone concentration, cytosolic oestrogen receptor exhibited a replenishment phase between 12 and 48 h. Although pharmacological levels of serum progesterone (0·47± 0·02μmol/l) significantly suppressed the level of occupied nuclear oestrogen receptor at 12 h, the level increased subsequently at 24 and 36 h and was equivalent to the control value (oestradiol alone) by 48 h. At a mean serum concentration of 0·18 ± 0·02 or 0·10 ± 0·01 μmol/l, the level of occupied nuclear oestrogen receptor was also suppressed significantly at 12 h, but to a lesser degree. These results show that progesterone decreases the concentration of occupied nuclear oestrogen receptor in the rat uterus and that the duration and extent of suppression of occupied nuclear oestrogen receptor is related to the serum progesterone concentration.
Journal of Endocrinology (1989) 121, 101–107
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Search for other papers by L A Salamonsen in
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Abstract
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.
Journal of Endocrinology (1995) 147, 235–244
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SUMMARY
The uterine fluid of mice killed 2–6 hr after coitus and ovulation amounted to about 0·1 ml. and contained about 20 million spermatozoa and virtually no leucocytes. By 14–18 hr after coitus the leucocytes had increased to about 25 million and the spermatozoa had decreased to about 11 million, most of which were undergoing phagocytosis. Approximately 20 hr after coitus the uterine contents are apparently evacuated, in spite of the continued presence of a copulation plug. Phagocytosis of spermatozoa was also observed in rats but was much less extensive; this is considered to be because evacuation takes place sooner after ovulation, though still about 20 hr after coitus. The phagocytes were nearly all polymorphonuclear leucocytes.
Leucocytic invasion of the uterine lumen seems to occur mainly because of the distension of the uterus with fluid and not because spermatozoa are present. No evidence was obtained that either spermatozoa or leucocytes pass from the lumen into the uterine wall.
