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At least 631 records · Page 35Linked to original sources
PubMed1996

Messenger ribonucleic acid levels of collagenase (MMP-13) and matrilysin (MMP-7) in virgin, pregnant, and postpartum uterus and cervix of rat.

Evidence indicates that matrix metalloproteinases (MMPs) are essentially involved in the postpartum involution of the uterus. As little information exists about the gene regulation of those MMPs in the uterus, this study aimed to characterize the time course of messenger RNA (mRNA) levels of rat collagenase (MMP-13) and matrilysin (MMP-7) in virgin, late pregnant (18th and 21st day), and postpartum rats (1, 2, 3, and 4 days postpartum). Rat collagenase (MMP-13) mRNA levels were very low in virgin and pregnant animals, but increased transiently 30-fold postpartum, reaching a maximum on the second day postpartum. The temporal course of mRNA levels of matrilysin (MMP-7) shows similarity with that of collagenase mRNA levels, but at any stage the abundance of matrilysin mRNA was at least 100-fold higher than that of collagenase. In virgin animals, matrilysin mRNA levels were dependent on the estrous cycle, being 3- to 4-fold higher in the estrous and diestrous stages than during metestrus. MMP-7 shows an approximately 25-fold induction when comparing the mRNA levels in late pregnancy and 2 days postpartum. In cervexes of virgin, pregnant, and postpartum groups, collagenase mRNA was not detectable. Matrilysin in cervix shows temporal mRNA expression similar to that in uterus, with a maximum on day 1 postpartum. In cervix, we found a 14-fold induction when comparing levels in late pregnancy and those 1 day postpartum. Taken together, our findings suggest that the increased activity of MMPs in the postpartum uterus is due to a strong increase in the mRNA levels of MMP-13 and MMP-7.

Animals↗
PubMed1996

Impaired estrogen action in the uterus of insulin-like growth factor binding protein-1 transgenic mice.

Insulin-like growth factor-I (IGF-I) has been implicated as autocrine/paracrine mediator of estrogen action in the rodent uterus. Here, we examined the effects of 17-beta estradiol (E2), epidermal growth factor (EGF), and IGF-I on DNA synthesis in the uterus of ovariectomized (ovex) transgenic mice (Tg), which overexpress rat insulin-like growth factor binding protein-1 (IGFBP-1). Litter size was significantly reduced in Tg mice compared with wild-type mice. Immunohistochemical studies localized the expression of the transgene to the luminal and glandular epithelium. In addition, rat IGFBP-1 immunoreactivity was present in luminal secretions. E2-induced uterine DNA synthesis as measured by methyl-3H thymidine incorporation, was significantly reduced in ovex Tg mice; 4.77 +/- 0.59 and 4.97 +/- 0.53 for Tg strains 57C and 277A, respectively, compared with 8.65 +/- 0.73 fmol/microgram of DNA for Wt mice. Similarly, uterine weight after three daily injections of E2 was reduced in Tg mice compared with Wt mice; 2.85 +/- 0.39 vs. 4.23 +/- 0.26 mg/g BW, P < 0.01. Semiquantitative RT-PCR assays were used to demonstrate changes in uterine IGF-I messenger RNA (mRNA) and EGF mRNA abundance after administration of E2. An approximately 3-fold increase in IGF-I mRNA abundance was seen 6 h after E2 in both Tg and Wt mice. Over the same time course, little change was seen in EGF mRNA levels, which were similar in Tg and Wt mice. After 3 days of E2 treatment, an increase in EGF mRNA was apparent in Wt mice but not in Tg mice. The uterine DNA response to both IGF-I and EGF was significantly attenuated in Tg mice compared with Wt mice. The data reported here together with previous reports of E2 regulation of IGF-I and IGFBP-1 expression in uterus support the hypothesis that the IGF-I is a mediator of estrogen action in the uterus. In addition attenuation of the EGF response in the uterine tissue of Tg mice suggests that this response is also mediated, in part, by IGF-I.

Animals↗
PubMed1997

Prostaglandin E2 receptor subtype EP2 gene expression in the mouse uterus coincides with differentiation of the luminal epithelium for implantation.

Among the PGs, PGE2 is considered especially important for implantation and decidualization. Four major PGE2 receptor subtypes, EP1, EP2, EP3, and EP4, mediate various PGE2 effects via their coupling to distinct signaling pathways. Previously, we have shown that the EP1, EP3, and EP4 genes are expressed in the periimplantation mouse uterus in a spatio-temporal manner, suggesting compartmentalized actions of PGE2 during this period. In this study, we examined the expression of the EP2 gene in the mouse uterus during the periimplantation period (days 1-8) and during experimentally induced progesterone (P4)-maintained delayed implantation and its resumption by 17beta-estradiol (E2). We also examined its regulation in the uterus by ovarian steroid hormones. Our results establish that EP2 messenger RNA (mRNA) is expressed exclusively in the luminal epithelium primarily on day 4 (the day of implantation) and day 5 (early implantation) of pregnancy. In (P4)-maintained delayed implanting mice, EP2 mRNA was present in the luminal epithelium, and the expression was further enhanced regardless of the location of the blastocysts after reinitiation of implantation. This observation suggests little or no embryonic influence in regulating EP2 expression and, instead, shows its regulation by P4 and E2. Indeed, treatment with E2 and/or P4 exhibited unique regulation of this gene. The treatment of adult ovariectomized mice with E2 down-regulated the basal levels of EP2 mRNA, whereas that with P4 up-regulated its levels in the luminal epithelium. The up-regulation of EP2 mRNA levels by P4 was further augmented by superimposition of the E2 treatment, suggesting a synergistic interaction between E2 and P4 in regulating this gene in the uterus. Collectively, the results suggest that EP2 could be a potential mediator of PGE2 actions in regulating luminal epithelial differentiation and serve as a marker for uterine receptivity for implantation.

Animals↗
PubMed1997

Differential expression of the erbB2 gene in the periimplantation mouse uterus: potential mediator of signaling by epidermal growth factor-like growth factors.

Ligand-receptor signaling with the epidermal growth factor (EGF) family of growth factors in the uterus and embryo is considered to be important for implantation. The EGF family includes EGF, transforming growth factor-alpha, heparin binding-EGF, amphiregulin, beta-cellulin, epiregulin, and heregulins, whereas the receptor family (the erbB genes) consists of erbB1 (EGF-receptor, EGF-R), erbB2, erbB3, and erbB4. Interactions of uterine EGF-R with EGF-like ligands have been examined, but limited information is available regarding the status of other receptor subtypes. Thus, we examined the expression of the erbB2 gene in the mouse uterus during the periimplantation period (days 1-8 of pregnancy) and after 17 beta-estradiol and/or progesterone stimulation. Northern blot hybridization detected two transcripts (approximately 4.0 and 5.0 kb) of erbB2 messenger RNA (mRNA) in day 1-8 uterine polyadenylated RNA samples. In situ hybridization experiments showed unique uterine cell-specific erbB2 mRNA distribution. On days 1-4, unlike the full-length erbB1 mRNA which is not expressed in the uterine epithelium, the erbB2 mRNA was detected primarily in epithelial cells; the day 1 uterus showed the highest accumulation. On day 5, the epithelium and the decidualizing stromal cells around the implanting blastocyst exhibited accumulation of this mRNA. On days 6-8, the accumulation persisted in the epithelium at both the implantation and interimplantation sites in addition to modest levels of signals in the secondary decidual zone. On days 7 and 8, accumulation of the erbB2 mRNA was also prominent in the trophoblastic giant cells. Western blotting detected a predicted protein of 185 kDa in day 4 uterine membrane preparations. Results of immunocytochemistry demonstrated colocalization of the erbB2 protein with its mRNA in the periimplantation uterus. The uterine ErbB2 underwent phosphorylation by several members of the EGF family. Treatment of adult ovariectomized mice with 17 beta-estradiol, but not progesterone, up-regulated the expression of the erbB2 mRNA by more than 3.5-fold, as determined by quantitative reverse transcription-PCR, and this increase was limited to the epithelium, as revealed by in situ hybridization. Collectively, the results place ErbB2 as a potential candidate receptor subtype for interaction with the EGF-related ligands in epithelial cell proliferation/differentiation during the preimplantation period and stromal cell proliferation/decidualization during the postimplantation period.

Amino Acid Sequence↗
PubMed1998

Immunolocalization of 11beta-hydroxysteroid dehydrogenase types 1 and 2 in rat uterus: variation across the estrous cycle and regulation by estrogen and progesterone.

Glucocorticoid hormone action in several target tissues is dependent not only on the expression of the glucocorticoid receptor, but also on that of the 11beta-hydroxysteroid dehydrogenase (11betaHSD) enzymes, 11betaHSD-1 and -2. In the uterus, glucocorticoids can exert inhibitory effects on a range of important functions, particularly in relation to the effects of estrogen. Therefore, the present study examined immunolocalization of the two 11betaHSD enzymes in the rat uterus at each stage of the estrous cycle and after ovariectomy with or without estrogen/progesterone replacement. In cycling rats 11betaHSD-1 was localized to luminal and glandular epithelial cells and to eosinophils in both the endometrial stroma and myometrium. In contrast, 11betaHSD-2 immunostaining was localized to endometrial stromal cells and myometrial cells, with no staining evident in epithelial cells or eosinophils. Immunostaining for both enzymes was cycle dependent, being maximal at proestrus and minimal at diestrus. Western blot analysis of whole uterus at proestrus showed the presence of 34- and 40-kDa immunoreactive species for 11betaHSD-1 and -2, respectively. These immunoreactive signals were almost abolished by ovariectomy, but this effect was reversed for both enzymes by estrogen replacement with or without progesterone. These effects of ovariectomy and steroid replacement were confirmed by immunocytochemical analysis, with the exception that progesterone appeared to enhance the stimulatory effects of estrogen on 11betaHSD-2 specifically within the endometrial stroma. In conclusion, these results establish the presence of both 11betaHSD-1 and -2 in the nonpregnant rat uterus and show distinct distributions for the two enzymes and cyclic variation related to positive regulation by ovarian steroids. The physiological implications of these patterns of 11betaHSD expression will ultimately depend on the reaction direction for each enzyme, but 11betaHSD-2 is likely to limit disruptive effects of glucocorticoids on the endometrial stroma, and 11betaHSD-1 may then serve to selectively reactivate glucocorticoids in epithelial cells.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1999

Signaling between the placenta and the uterus involving the mitogen-regulated protein/proliferins.

The aim of this investigation was to examine signaling between the placenta and uterus during pregnancy. To do this, we determined the tissue messenger RNA and protein levels of members of a glycopeptide hormone family known to stimulate the proliferation of uterine cells and related these levels to the growth of the uterus during pregnancy in the mouse. This hormone family is known as mitogen-regulated protein (MRP); alternatively proliferin (PLF). Three mrp/plf genes, plf1, mrp3 and mrp4, are expressed by the placenta with different developmental profiles. The major increase of about 4-fold in DNA content of the uterus occurs between days 9 and 14 when MRP/PLFs are present in the placenta. By contrast, the gestational changes in estradiol-17beta levels in placental and uterine tissues and in circulation do not correlate with the period of uterine growth. The previously reported mitogenic activity of the MRP/PLFs and their gestational profiles suggest that one or more of these proteins stimulates uterine proliferation during gestation. Evidence is also presented that expression of MRP3 and/or PLF1, but not MRP4, is negatively regulated by feedback from the uterus. Our results are consistent with the hypothesis that MRP/PLFs stimulate uterine proliferation in vivo and that a uterine factor shuts off PLF1 and/or MRP3 synthesis in the latter half of gestation.

Amniotic Fluid↗
PubMed2001

The type 2 iodothyronine deiodinase is expressed in the rat uterus and induced during pregnancy.

Thyroid hormones are of considerable importance for vertebrate reproductive function and during development. To further assess the role of these compounds in this capacity, we examined the expression pattern of the type 2 iodothyronine deiodinase (D2), which converts T(4) to the more active hormone T(3), in the rat uterus in both the nonpregnant and the pregnant state. D2 activity was identified as the predominant, if not only, 5'-deiodinase in the nonpregnant rat uterus. The expression of D2 messenger RNA was located by in situ hybridization to the endometrial stromal cells, where the signal was particularly enriched in the region adjacent to the epithelial cells of the uterine lumen. During pregnancy, D2 activity increased, peaking on day 17 of gestation (embryonic day 17). At that time, uterine D2 activity exceeded that in the placenta, as well as that in the fetal tissues. In the earlier stages of pregnancy before placental formation (e.g. embryonic days 10-11), D2 messenger RNA in the rat uterus was located outside the decidual tissue, which was observed, as in previous studies, to highly express the inactivating type 3 deiodinase. In summary, the rat uterus, particularly during pregnancy, seems to be a site of active thyroid hormone metabolism, presumably designed to maintain the optimal thyroid hormone environment for both the fetus and the maternal uterine tissue.

Animals↗
PubMed1981

Prolactin and relaxin: antagonism on the spontaneous motility of the uterus.

Prolactin (PRL) and Relaxin (RXL) are present in human decidua at term. In previous experiments we observed that the inhibition of spontaneous uterine contractions produced by decidual RLX was masked or absent if the samples were contaminated with PRL. The present study reports the effect of purified human PRL and of sera from hyperprolactinemic patients on the motility of the uterus in vitro. Also, we studied the effect of RLX on the uterus after exposure to PRL. High-PRL sera and purified human PRL produced prompt increases in the frequency and the amplitude of the spontaneous contractions of the rat uterus. PRL antagonized RLX both when the uterus was exposed first to RLX and then to PRL and when it was exposed first to PRL and then to RLX.

Animals↗
PubMed2004

Stability of A+U-rich element binding factor 1 (AUF1)-binding messenger ribonucleic acid correlates with the subcellular relocalization of AUF1 in the rat uterus upon estrogen treatment.

The nucleocytoplasmic shuttling protein, A+U-rich element binding factor 1 (AUF1), is one of the RNA-binding proteins that specifically bind adenylate-uridylate rich elements (AREs) in mRNA 3'-untranslated regions (UTRs), and acts as a regulator of ARE-mediated mRNA degradation in the cytoplasm. We previously reported that in the female rat uterus, the levels of specific AUF1 isoform mRNAs (p40/p45) were increased by 17 beta-estradiol (E2) treatment. Therefore, we examined the role of AUF1 in the regulation of E2-mediated mRNA turnover in the rat uterus. We identified ABIN2 and Ier2/pip92 mRNAs as candidate targets of AUF1 in the rat uterus. We found that AUF1-binding elements were present in the 3'-UTR of both mRNAs and that the 3'-UTRs functioned as mRNA turnover regulatory elements. In the ovariectomized rat uterus, the nucleocytoplasmic localization of AUF1p40/p37 isoform proteins was regulated by E2. We also found that cytoplasmic AUF1-bound mRNA levels changed coincidentally with the cytoplasmic levels of AUF1p40/p37. Finally, we confirmed that the subcellular localization of AUF1p40 controlled the stability of target mRNAs in vitro, such that cytoplasmically localized AUF1p40 led to marked mRNA stabilization, whereas nuclear-localized AUF1p40 stabilized target mRNA only slightly. These results suggested that E2-inducible ARE-containing gene transcripts are regulated, at least in part, via mRNA stabilization through the nucleocytoplasmic relocalization of AUF1.

3' Untranslated Regions↗
PubMed1988

Estrogen induces expression of c-fos and c-myc protooncogenes in rat uterus.

Estrogen stimulates DNA synthesis and cell proliferation in the luminal and glandular epithelia of rodent uterus. We tested the hypothesis that the mitogenic effect of estrogen occurs via activation of the expression of cellular proto-oncogenes by measuring the rate of transcription of 20 proto-oncogenes (abl, bas, erb-A, erb-B, ets, fms, fos, fps/fes, mos, myb, myc, N-myc, raf, Ha-ras, Ki-ras, N-ras, rel, sis, src, and B-lym) in the uterus of ovariectomized rats before and after injection of estrogen. c-onc transcriptional activity was monitored both by an in vitro transcription assay on isolated nuclei (run-on) and by analysis of mature mRNA. c-fos and c-myc proto-oncogenes were found to respond to estrogen with increased expression: c-fos within 30 min, with a first, sharp peak at 2 h and c-myc within 1.5 h, with a first, broad peak at 4-6 h. DNA synthesis start to increase in the uterus 13 h after estrogen injection and show a first peak at 24 h. In the liver and muscle of the same animals there is neither elevation of c-fos and c-myc expression nor increase of DNA synthesis. The kinetics of the induction by estrogen of c-fos gene expression in the uterus parallels the rate of formation of active nuclear estrogen-receptor complex. Furthermore, the ability of estrogen to induce c-fos mRNA was not abolished by the protein synthesis inhibitor cycloheximide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Proenkephalin gene expression in the primate uterus: regulation by estradiol in the endometrium.

Proenkephalin mRNA has previously been shown to be expressed in the rodent uterus with varying levels during the estrous cycle. To examine for the potential regulation of proenkephalin gene expression by steroid hormones in a primate displaying a menstrual cycle and to define the functional tissue within the uterus expressing this transcript, we have used Northern blot analysis of extracted RNA from isolated uterine tissue subtypes from normal adult rhesus macaques obtained during the menstrual cycle and from ovariectomized females under different physiological steroid hormone treatments. A strong band of proenkephalin mRNA of 1.3 kilobases was detected almost exclusively in the proliferative endometrium from monkeys in the follicular phase of the cycle. No proenkephalin mRNA was detected in secretory endometrium obtained from monkeys in the luteal phase. When ovariectomized macaques were implanted with silastic capsules of 17 beta-estradiol, proenkephalin mRNA was detected in the endometrium but not the myometrium of the estradiol-treated animals. No proenkephalin mRNA was detected in ovariectomized control animals. Under these conditions, we were unable to detect proenkephalin mRNA in ovariectomized macaques implanted with separate silastic capsules of 17 beta-estradiol and progesterone or in decidual tissue from early or late pregnancy. These results suggest that in the primate uterus 1) proenkephalin mRNA is expressed primarily in the endometrium of the uterus, 2) expression of the proenkephalin gene is regulated by 17 beta-estradiol in the endometrium, and 3) this effect of estradiol is antagonized by progesterone.

Animals↗
PubMed2000

Dysregulation of EGF family of growth factors and COX-2 in the uterus during the preattachment and attachment reactions of the blastocyst with the luminal epithelium correlates with implantation failure in LIF-deficient mice.

Various mediators, including cytokines, growth factors, homeotic gene products, and prostaglandins (PGs), participate in the implantation process in an autocrine, paracrine, or juxtacrine manner. However, interactions among these factors that result in successful implantation are not clearly understood. Leukemia inhibitory factor (LIF), a pleiotropic cytokine, was shown to be expressed in uterine glands on day 4 morning before implantation and is critical to this process in mice. However, the mechanism by which LIF executes its effects in implantation remains unknown. Moreover, interactions of LIF with other implantation-specific molecules have not yet been defined. Using normal and delayed implantation models, we herein show that LIF is not only expressed in progesterone (P4)-primed uterine glands before implantation in response to nidatory estrogen, it is also induced in stromal cells surrounding the active blastocyst at the time of the attachment reaction. This suggests that LIF has biphasic effects: first in the preparation of the receptive uterus and subsequently in the attachment reaction. The mechanism by which LIF participates in these events was addressed using LIF-deficient mice. We observed that while uterine cell-specific proliferation, steroid hormone responsiveness, and expression patterns of several genes are normal, specific members of the EGF family of growth factors, such as amphiregulin (Ar), heparin-binding EGF-like growth factor (HB-EGF), and epiregulin, are not expressed in LIF(-/-) uteri before and during the anticipated time of implantation, although EGF receptor family members (erbBs) are expressed correctly. Furthermore, cyclooxygenase-2 (COX-2), an inducible rate-limiting enzyme for PG synthesis and essential for implantation, is aberrantly expressed in the uterus surrounding the blastocyst in LIF(-/-) mice. These results suggest that dysregulation of specific EGF-like growth factors and COX-2 in the uterus contributes, at least partially, to implantation failure in LIF(-/-) mice. Since estrogen is essential for uterine receptivity, LIF induction, and blastocyst activation, it is possible that the nidatory estrogen effects in the P4-primed uterus for implantation are mediated via LIF signaling. However, we observed that LIF can only partially resume implantation in P4-primed, delayed implanting mice in the absence of estrogen, suggesting LIF induction is one of many functions that are executed by estrogen for implantation.

Animals↗
PubMed1981

Effects of smooth muscle relaxant (aspaminol) on Ca-uptake by mitochondrial and microsomal fractions from rat uterus.

A smooth muscle relaxant, Aspaminol (1,1-diphenyl-3-piperidinobutanol hydrochloride) relaxed a KCl-depolarized rat uterus and shifted a dose response curve of CaCl2 towards higher doses. Asparminol, a teritary amine, may penetrate into the KCl-depolarized muscle cells. In order to study mechanisms for relaxation of the KCl-depolarized rat uterus by Aspaminol, effects of Aspaminol on Ca-uptake by mitochondrial and microsomal fractions from the rat uterus were studied. Aspaminol inhibited Ca-uptake by both fractions. Inhibition of Ca-uptake by the mitochondrial fraction seems to increase intracellular Ca2+. Therefore, inhibition of Ca-uptake by the mitochondrial fraction is considered to be not associated with relaxation of uterus induced by Aspaminol. Since the microsomal fraction is known to form microsacs, the microsomal fraction was used as smooth muscle models. Inhibitory effect of Aspaminol on Ca-uptake by the microsomal fraction suggest a decrease in the intracellular concentration of Ca2+ of the uterine smooth muscle relaxed under the influence of Aspaminol.

Animals↗
PubMed2006

Calbindin-D9k mRNA expression in the rat uterus following exposure to methoxychlor: a comparison of oral and subcutaneous exposure.

Calbindin-D(9k) (CaBP-9k) is a cytosolic calcium-binding protein that is induced by estrogenic compounds possibly through estrogen receptors. We compared CaBP-9k mRNA expression in the uterus with uterotrophic response in immature rats exposed to methoxychlor (MC), an environmental chemical with estrogenic activity. MC was orally or subcutaneously administered to 3-week-old female Sprague-Dawley rats for 3 days. The weights of the uterus and vagina significantly increased in the oral treatment group at a dose of 50, 100 and 200 mg/kg, but those of the subcutaneous (SC) treatment group only increased at 200 mg/kg. Northern blot analysis showed that CaBP-9k mRNA expression was significantly induced in a dose-dependent manner at doses of 50, 100 and 200 mg/kg/day in the oral treatment group. SC administration of MC induced significant expression at only a dose of 200 mg/kg/day; this was similar to the uterotrophic response. MC has an estrogenic effect on the uterus as shown by the increase in weight and induction of CaBP-9k mRNA expression, which were much greater following exposure via oral gavage than via the SC route. The strong correlation between the results of in vivo uterotrophic assay and CaBP-9k mRNA expression suggests that CaBP-9k mRNA expression in the rat uterus may be used as an early gene marker for detection of the estrogenic effects of putative environmental chemicals.

Administration, Oral↗
PubMed2003

Expression of estrogen receptor alpha and beta in the uterus and vagina of immature rats treated with 17-ethinyl estradiol.

The action of estrogen on target organs has been actively studied with the discovery of estrogen receptor (ER) beta. This study was carried out to examine the expression of ERalpha and ERbeta in the uterus and the vagina of immature Sprague-Dawley rats treated with 17-ethinyl estradiol (EE). Twenty days old rats were subcutaneously treated with EE at the doses of 0 (vehicle control), 0.03, 0.3, 1.0, 3.0, and 10.0 microg/kg/day for three consecutive days. The treatment of EE at the doses of 0.3, 1.0, 3.0 and 10.0 microg/kg/day significantly increased the weights of the uterus and vagina of rats (p<0.01) and retained fluid in the uterus of rats. At the high doses of 3.0 and 10.0 microg/kg/day, the treatment of EE caused an increase in the uterine height, hypertrophy, and a decrease in the expression of ERalpha and ERbeta in the uterine luminal and glandular epithelium. The treatment of EE at the doses of 3.0 and 10.0 microg/kg/day also caused cornification and a decrease in the expression of ERalpha and ERbeta in the vaginal epithelium. These results suggest that the EE treatment decrease the expression of ERalpha and ERbeta in the uterus and vagina of immature rats and that may be associated with the morphological changes such as increase in the uterine height, hypertrophy of the uterine epithelium, and cornification of the vagina.

Animals↗
PubMed2004

Long-term sensitivity of uterus and hypothalamus/pituitary axis to 17beta-estradiol is higher than that of bone in rats.

UNLABELLED: We examined the long-term sensitivity of uterus and bone to low-dose 17beta-estradiol in a 4-month experiment in OVX rats and found that a dose of estradiol that fully protected against uterine atrophy did not protect against bone loss. Our results suggest higher estrogen sensitivity of the uterus compared with bone. INTRODUCTION: Estrogen is essential for the function of reproductive tissues and for the normal acquisition and maintenance of bone mass in females. This study was designed to examine the long-term sensitivity of the uterus and bone to low-dose estrogen. MATERIALS AND METHODS: In preliminary experiments, we determined the lowest subcutaneous dose of 17beta-estradiol able to fully protect against uterine atrophy in ovariectomized (OVX) rats. This dose was found to be 1.5 microg/kg, given five times per week. Subsequently, groups of sham-operated (SHAM) or OVX 6-month-old rats (n = 8 each) were subcutaneously injected with vehicle or 1.5 microg/kg 17beta-estradiol five times per week. All animals were killed 4 months after surgery. Serum osteocalcin and urinary deoxypyridinoline were measured as biochemical markers of bone turnover. Bones were analyzed by bone histomorphometry and pQCT. RESULTS AND CONCLUSIONS: Our study clearly showed that a dose of estradiol that restores physiological estradiol serum levels, fully maintains uterine weight in OVX rats at the SHAM control level, and suppresses serum follicle-stimulating hormone (FSH) by 67% relative to OVX vehicle controls does not provide significant protection against OVX-induced bone loss at different cancellous and cortical bone sites. We conclude that the long-term sensitivity of the uterus and the hypothalamus/pituitary axis to 17beta-estradiol is higher than that of bone in rats.

Amino Acids↗
PubMed1981

Distribution of oestrogen-induced peroxidase in the rat uterus.

The activity of oestrogen-induced peroxidase in sections along the uterus of normal and mammary tumour-bearing adult rats was measured. Oestradiol increased the activity of this enzyme in the cervix as well as in other parts of the uterus in ovariectomized or immature rats. Peroxidase activity per mg protein was twice as high in the cervix as in the rest of the uterus where it was evenly distributed along both horns. The concentrations of oestrogen receptors in the cytosol and nucleus in each uterine horn and in the cervix was also determined and found to be lower in the cervix than in other sections of the uterus.

Animals↗
PubMed1982

Prostaglandin production by the rabbit uterus and placenta in vitro.

Endogenous concentrations of prostaglandin (PG) F-2 alpha in the rabbit uterus were higher on Day 17 of pseudopregnancy than on Days 4, 7 and 11 of pseudopregnancy and Day 17 of pregnancy. These differences are consistent with the findings reported previously that the output of PGF-2 alpha from the rabbit uterus is higher on Day 17 of pseudopregnancy than on earlier days of pseudopregnancy and Day 17 of pregnancy. Uterine homogenates synthesized PGs and, of the 3 PGs measured, 6-oxo-PGF-1 alpha was the major product. There were no differences in the amounts of any one PG synthesized during pseudopregnancy. 'unstretched' uterine tissue from Day-17-pregnant rabbits produced quantities of PGs similar to those of uterine tissue from Day-17-pseudopregnant rabbits. However, 'stretched' uterine tissue from Day-17-pregnant rabbits produced more 6-oxo-PGF-1 alpha and PGE-2, but not PGF-2 alpha, than did 'unstretched' tissue or pseudopregnant uterine tissue from Day-17 rabbits. PG production by the fetal placenta was higher than that by the maternal placenta. PGE-2 and 6-oxo-PGF-1 alpha were the major PGs produced by the fetal and maternal placentae, respectively. Metabolism of PGF-2 alpha required NAD+ and metabolism by the placenta was greater than that by the uterus. Compounds less polar and more polar than PGF-2 alpha were produced, although the production of more polar metabolites appeared to require a period of progesterone priming of the uterus.

6-Ketoprostaglandin F1 alpha↗