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At least 865 records · Page 48Linked to original sources
PubMed1988

Classification of angiotensin receptors in rat isolated uterus, portal vein, and aorta using a slowly dissociating antagonist [Sar1,Ile8]ANG II for receptor blockade.

Receptor blockade with the slowly dissociating angiotensin (ANG) antagonist, [Sar1,Ile8]ANG II, was used to determine dissociation constants (Kd) for angiotensins II and III at receptors in rat isolated uterus, portal vein and aorta. The Kd values obtained were 1) ANG II: uterus, 2.2 +/- 1.2 X 10(-8)M; portal vein, 8.5 +/- 2.5 X 10(-9)M; aorta, 7.8 +/- 1.7 X 10(-9)M; and 2) ANG III: uterus, 5.7 +/- 1.7 X 10(-7)M; portal vein, 4.5 +/- 3.1 X 10(-7)M; aorta, 1.4 +/- 0.5 X 10(-7)M. For either ANG II or ANG III, there were no clearly significant differences in the Kd values obtained for the smooth muscle tissues investigated. The derived Kd values provided a relationship between receptor occupancy and response that illustrated that the two peptides had similar efficacies in all three tissues. The method provides a quantitative description of receptors and suggests that the angiotensin receptor is of the same type in all three tissues.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1996

Comparison of the effects of bradykinin and related compounds on isolated mouse and human uterus.

The purpose of this study was to investigate and compare the response of the isolated human myometrium (non-pregnant donors) and mouse uterus to bradykinin (BK), Lys-BK and des-Arg9-BK (+/-2.79 microM indomethacin). The uterine strips were set up for superfusion using Kerbs' solution. On the human myometrium the responses to BK and Lys-BK were biphasic and consisted of an increase in myometrial tension which was followed by a period of inhibition of myogenic activity. Des-Arg9-BK evoked a monophasic contractile response. On the mouse uterus the responses to BK, Lys-BK and des-Arg9-BK were monophasic and contractile only. On both of the tissues the contractile responses to BK and Lys-BK were bell shaped and indomethacin abolished the bell-shaped part of the dose response curves. The response to des-Arg9-BK and the inhibitory response to BK and Lys-BK, on the human tissue, was also significantly reduced in the presence of indomethacin. The results of this study suggest that the human and mouse uterus do posses kinin receptors of the B2 type but on human myometrium these are biphasic responses.

Animals↗
PubMed1982

Histological and immunological studies of post implantation death of Mus caroli embryos in the Mus musculus uterus.

Mus caroli blastocysts surgically transferred to the Mus musculus uterus implant and develop successfully during the first 9.5 days of gestation. At this time, the trophoblast giant cell area becomes infiltrated with lymphocytes and, subsequently, massive hemorrhage occurs, associated with embryo death. This process is specific for the xenogeneic embryos and does not affect adjacent allogeneic embryos present in the same uterus. Cells taken from the resorbing tissues contain a population of large Thy 1+, Lyt 1+, Lyt 2+ cytotoxic cells capable of lysing Mus caroli concanavalin A blasts in vitro. It is suggested that failure of the Mus caroli embryos in the Mus musculus uterus is mediated by the maternal immune system and that the xenogeneic blastocyst transfer system provides a suitable animal model system for studies of mechanisms that prevent rejection of the fetal allograft.

Animals↗
PubMed1990

Immunoregulatory activity of cells from lymph nodes draining the uterus of allopregnant mice.

The presence of a local immunosuppressive environment in the vicinity of the developing fetus has been suggested to explain survival of the semi-allogeneic fetus in a potentially hostile maternal immunologic environment. The presence of nonspecific suppressor cells in the uterus of pregnant mice has been well-documented. It has been suggested that the local immunosuppressive environment extends to the lymph nodes draining the uterus of pregnant mice. Studies undertaken to investigate this hypothesis have provided conflicting data. The current study was performed as an attempt to resolve some of the controversial results obtained from previous studies and to characterize more extensively the nature of lymph node suppressor cells. Our results clearly demonstrated that neither specific nor non-specific immunosuppression was expressed within lymph nodes draining the uterus of allopregnant mice. Cells obtained from draining lymph nodes consistently exhibited a normal capacity to respond to alloantigens whether by proliferation or through cytotoxic T lymphocyte (CTL) generation. We conclude that immunosuppression fails to develop in draining lymph nodes during pregnancy and therefore plays little or no role in controlling the development of antifetal immune responses.

Animals↗
PubMed1992

Proto-oncogene erbA expression and increased abundance of progesterone receptors in the mouse uterus after passive immunisation against progesterone before implantation.

Passive immunisation with a monoclonal anti-progesterone antibody (DB3) prevents pregnancy in the mouse, and antibody is localised in the endometrium before the onset of implantation. BALB/c female mice were injected intraperitoneally with 9 nmol of DB3 (a dose known to cause 100% infertility) 32 h post coitum, and the uterus was removed at various times after injection. Using a monoclonal anti-progesterone receptor antibody (PR6), expression of progesterone receptors was found to be abundant in uterine tissue of DB3-treated mice; this was associated with substantial progesterone receptor mRNA levels and with maximum localisation of DB3 antibody as detected by anti-idiotype antibody. Control animals treated with an equal amount of the mouse myeloma protein P3 showed very low levels of progesterone receptor in the uterus. DB3 treatment also affected uterine expression of the proto-oncogene erbA product (which shows primary sequence homology with the progesterone receptor) as revealed by specific antiserum to the ERBA protein and by in situ hybridisation with a cDNA probe to v-erbA. Time-course studies indicated that the erbA gene was expressed at a high level before progesterone receptor expression increased, that its expression was dependent on the presence of the embryo and that erbA expression persisted longer in DB3-treated females. The observations suggest that anti-progesterone immunisation has a direct effect within the uterus, involving persistence of proto-oncogene erbA expression (which itself may represent an early maternal response to pregnancy) and increased progesterone receptor levels resulting from an unopposed oestrogen effect derived from local ligand withdrawal.

Amino Acid Sequence↗
PubMed1983

Metabolic factors regulating the generation of prostaglandins E1 and E2 by isolated rat uterus.

The generation and output of PGE2 and PGE1 by isolated rat uterus incubated with or without glucose as well as the influence of different metabolic substrates and selective enzyme inhibitors on tissue formation and release of PGE material of the 1 and 2 series, were explored. The output of PGE2 was comparable with glucose, fructose, lactate or pyruvate as the substrate but diminished significantly in citrate-containing solution. In substrate-free media uteri released more PGE2 than in the presence of glucose or other substrates. The PGE1 liberated was similar in glucose, fructose, lactate or pyruvate and decreased significantly in citrate or without substrate. 2-deoxy-D-glucose (2-DG), fluoride or arsenite failed to alter significantly the release of PGE2 whereas 2,4-dinitrophenol (DNP) evoked augmentation. The uterus released less PGE1 after 2-DG or fluoride but not following the addition of DNP or arsenite. The results suggest that the synthesis and release of PGE2 and PGE1 in the isolated rat uterus appear to be selectively modulated by different tissue metabolic pathways.

Alprostadil↗
PubMed1983

Effect of treating ovariectomized guinea-pigs with estradiol and progesterone on basal and A23187-stimulated release of prostaglandins from the uterus superfused in vitro.

The outputs of PGF2 alpha, PGE2 and 6-oxo-PGF1 alpha from the uterus of ovariectomized guinea-pigs were all low (approximately 0.1 to 0.2 ng/min/uterine horn). PGF2 alpha was released in greatest quantities, followed by PGE2 and then by 6-oxo-PGF1 alpha. Progesterone treatment had no effect on PG output. Estradiol treatment increased PGF2 alpha output 7-fold, but increased PGE2 and 6-oxo-PGF1 alpha outputs only 1.7-fold and 2.9-fold, respectively. Estradiol treatment reversed the PGE2 to 6-oxo-PGF1 alpha ratio. Progesterone-priming before estradiol treatment potentiated the stimulatory effect of estradiol on PGF2 alpha release up to 2-fold, but had no such action on the stimulatory effect of estradiol on PGE2 and 6-oxo-PGF1 alpha release. Estradiol acting on a progesterone-primed uterus causes a relatively specific activation of PGF2 alpha synthesis and release. The physiological significance of this observation is discussed. A23187 stimulated PGF2 alpha release from all uteri irrespective of treatment. However, the magnitude of the response was much greater in those guinea-pigs which had received estradiol (either alone or with progesterone) than in those which had not. A23187 stimulated also 6-oxo-PGF1 alpha release, but to a much lesser extent, and had no effect on PGE2 release. Raising free intracellular Ca2+ levels in the uterus stimulates PGF2 alpha release and, to a lesser extent, 6-oxo-PGF1 alpha release, but the size of the response depends upon the hormonal status of the animal.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

The effect of ovarian steroids on prostaglandin F2 catabolism in ovariectomized rat uterus.

The effects of ovarian steroids, estradiol and progesterone, on the prostaglandin F2 (PGF2) catabolism in vitro in rat uterus were examined by using labeled PGF2. The formation of 13,14-dihydro-15-keto-PGF2 (13,14H2-15K-PGF2) from PGF2 was stimulated by a single injection of estradiol (10 micrograms) or progesterone (1 mg). A remarkable increase in the 13,14H2-15K-PGF2 formation was recognized at 12 hours after estradiol treatment and the formation reached the maximal level at 24 hours. Progesterone also raised the gradual increase of PGF2 catabolism at 24 and 48 hours. In the case of the simultaneous administration of estradiol and progesterone, the additive effect in the PGF2 catabolism was not observed at 24 hours after a single injection of steroids. However, the additive effect was observed by the repeated treatment (once a day for 3 days) of both estradiol (1 microgram) and progesterone (1 mg). These results indicate that PGF2 catabolism in rat uterus is accelerated by ovarian steroids, and also suggest that ovarian hormones closely take part in the regulation of the levels of PGF2 in rat uterus.

Animals↗
PubMed1984

Studies on the temporal pattern of prostaglandin synthesis in the uterus of the delayed implanting rat with or without implantation inducing stimuli.

The model of delayed implantation produced by injection of progesterone (P4) following hypophysectomy on day 3 of pregnancy, was used to study the temporal relationship between phospholipase A2 (PLA2) activity and endogenous concentrations and/or in vitro production of prostaglandins (PGs) in the rat uterus during the early phase of implantation. No definitive correlation between the endogenous concentration of uterine PGs and their in vitro production, or PLA2 activity, was found following various treatments. However, an interesting interaction between various treatments and PLA2 activity, as well as PG production, was evident within 0.5 h-4 h. The unaltered PLA2 activity and PG production in the uterus at 0.5 h and 4 h after the last injection of P4 only suggest that PLA2 is probably the limiting step in PG synthesis in the P4 dominated uterus. On the other hand, the depressed uterine PG production at 0.5 h, in the face of unaltered PLA2 activity, in P4-primed rats injected with an optimal dose of estradiol-17 beta (E2: 20 ng/rat, i.v.) suggests a reduction in PG synthetase activity with estrogen. Because PLA2 activity remained unchanged, the stimulation in PGE, and to some extent PGF, production at 0.5 h following superimposition of histamine on the E2 treatment appears to be mediated via stimulation of PG synthetase. The increase in PGE and PGF production at 4 h as compared to 0.5 h following E2 injection was accompanied by increased PLA2 activity. However, PGF production did not exceed that obtained with only P4. Addition of histamine to the P4 and E2 treatment potentiated the stimulation of PG production at 4 h without further elevation in PLA2 activity. A suboptimal dose of E2 (10 ng/rat, i.v.) failed to increase PLA2 activity and PG production, compared to those obtained with 20 ng/rat of E2. However, coadministration of histamine with the low dose of E2 increased PG production to the level found with the optimal dose of E2; this was achieved without a significant change in PLA2 activity. On the other hand, histamine did not reverse the inhibitory effect of dexamethasone on E2 stimulation of PLA2 activity and PG production. Taken together these results suggest that histamine induced potentiation of PG production in P4 and E2 treated rats is probably mediated via activation of PG synthetase activity. PLA2 activity was increased significantly at 8 h after the last injection of P4. However, this increase in activity was reflected in increased PGE, but not PGF production.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Multimolecular forms of oxytocinase activity in the human uterus and their inhibition by prostaglandins and cyclic GMP.

Oxytocinase (EC 3.4.11.3) activity was measured in uterine homogenates from pregnant and non-pregnant women using S-benzyl-L-cysteine-p-nitroanilide (BCN) and L-leucine-p-nitroanilide (LN) separately as substrates. There was no significant difference between the specific activity of the enzyme in the pregnant and non-pregnant uterus. The uterine homogenates were also subjected to gel filtration on Ultrogel AcA 22 column and two hydrolyzing activity peaks from the pregnant uterus (PUI, PUII) and three from the non-pregnant uterus (UI, UII, UIII) were obtained. Although the pattern of hydrolysis of the two substrates by the enzyme peaks was similar, the hydrolysis of LN was greater than that of BCN. PUII, UII and UIII showed higher affinity for the substrates than PUI and UI, and the affinity of all isoenzymes was significantly greater for LN than BCN. These uterine oxytocinases appeared to be metallo-aminopeptidases and were potently inhibited by Cu2+, Zn2+ and prostaglandins (PGs). Cyclic GMP (cGMP) and its 8-bromo derivative, however, inhibited only PUI and UI. The divalent cations and PGs were equipotent against the hydrolysis of both substrates, but cGMPs were more effective against BCN hydrolysis. All of these inhibitions depended on the pH of the incubation medium and types of the inhibition by PGs and cGMPs were mixed and uncompetitive respectively. The implications of these findings in relation to human parturition have been discussed.

Aminopeptidases↗
PubMed1990

Pituitary-related weight changes affecting the liver, uterus and adrenal glands of rats treated with hexoestrol and clomiphene in high doses.

The synthetic oestrogen hexoestrol, administered at 60 mg/kg/day for 4 days to female rats in 3 studies, caused the following mean changes in the relative weights of some of the principal organs: liver (+37%), spleen (-11%), adrenals (+43%), kidneys (+3%), pituitary (+23%), uterus (+49%), and ovaries (+13%). The heart weights showed no consistent changes. The mean relative organ weights of hypophysectomized, hexoestrol-treated rats did not differ significantly from those of untreated hypophysectomized controls. The latter animals had lower organ weights than sham-operated controls. Pretreatment with clomiphene citrate at dose levels of 20-60 mg/kg/day prevented in a dose-dependent manner most of the organ weight changes induced by hexoestrol. The exception was the adrenal weight, which was increased. Compared with controls, the mean relative organ weights of rats receiving clomiphene alone at 60 mg/kg/day differed as follows: liver (-18%), spleen (-17%), heart (-16%), adrenals (+7%), kidneys (-11%), pituitary (-13%), uterus (-25%), and ovaries (-4%). The changes affecting the liver, spleen, heart, kidneys and uterus were significant. Rats immunised with a monkey antiserum to rat growth hormone and treated with hexoestrol had significantly lower relative liver weights than did animals treated with hexoestrol alone. No other significant differences were observed. It is tentatively concluded that there is a mediating or co-operative pituitary influence involved in the significant hepatic, uterine and adrenal weight gains caused by hexoestrol. Clomiphene may act centrally to affect these organ weight changes and, indeed, may act at this level to (mainly) anti-organotrophic effect even in the absence of exogenous oestrogen. In the case of the hexoestrol-induced liver enlargement, the role of pituitary growth hormone is worth further investigation.

Adrenal Glands↗
PubMed1986

Induction of progesterone receptor by androgens in the mouse uterus.

The comparative abilities of 3 naturally occurring androgens to compete for [3H]estradiol-17 beta ([3H]E2)-binding sites in uterine cytosol and to induce uterotrophic responses in immature female mice have been investigated. 5 alpha-Androstane-3 beta,17 beta-diol (3 beta-diol), 5 alpha-androstane-3 alpha,17 beta-diol (3 alpha-diol) and 5-androstene-3 beta,17 beta-diol (delta 5-diol) are all effective at diminishing cytoplasmic [3H]E2 binding. Their relative effectiveness are in the order of 3 beta-diol greater than delta 5-diol = 3 alpha-diol. When these steroids were injected intramuscularly (two 100-200 micrograms injections) into immature female mice (21 days old), they induced similar elevations of uterine dry weight, water content, cytosolic estrogen (ER) and progesterone (PR) receptor contents, and nuclear ER content as did estradiol-17 beta (E2). 3 beta-Diol was the most effective steroid at inducing cytosolic and nuclear ER, and PR production in mouse uterus. Followed in effectiveness was delta 5-diol and 3 alpha-diol. Unexpectedly, 3 beta-diol was found to be more potent than E2 in stimulating uterine ER and PR increases. Nonetheless, the androgens are poorer stimulators of uterine dry weight increase and water retention than E2 is. These results indicate that the androgens may interact with the ER system in the uterus to bring about the uterotrophic responses and 3 beta-diol is a more estrogenic steroid than delta 5-diol and 3 alpha-diol in the mouse uterus.

Androgens↗
PubMed1987

Detection of estrogen receptor mRNA in human uterus.

We transcribed a cDNA clone of the human estrogen receptor (ER) with T7 RNA polymerase. The 32P-cRNA transcript complementary to ER mRNA was hybridized to poly(A)+ RNA from human uterus and revealed a single band of approximately 4.2 kilobases. No hybridization was seen with the cRNA probe of the opposite orientation. Hybridization of total RNA from calf and rat uterus yielded a single band at approximately 3.8 kilobases for both species. Total RNA from rat spleen did not hybridize. A 35S-labeled cRNA probe was prepared for in situ hybridization of ER mRNA in human uterus and spleen. Autoradiographic signal was present over endometrial epithelium, stromal cells of the lamina propria, and smooth muscle cells of the myometrium but was absent from sections of spleen. The ER mRNA hybridization label was located over cytoplasm and nuclei of uterine target cells.

DNA↗
PubMed1992

Calbindin-D9k mRNA is tightly regulated during the estrous cycle in the rat uterus.

Calbindin-D9k (CaBP-9k) is a cytosolic calcium binding protein with a molecular weight of 9000. CaBP-9k is mainly expressed in intestine, uterus and placenta, with intestinal levels controlled by vitamin D and uterine levels controlled by estrogens. CaBP-9k mRNA levels were measured in rat uterus throughout the estrous cycle. On the morning of proestrus, estrus and diestrus animals were sacrificed. Serum 17 beta-estradiol concentrations were determined using a radioimmunoassay. Whole uterus was used for preparation of total RNA. Northern blot analysis was performed to quantify CaBP-9k and beta-actin mRNA. CaBP-9k levels were highest at proestrus, dropped 10-fold at estrus and were not detectable at diestrus. beta-Actin levels did not change significantly throughout the estrous cycle. Peak 17 beta-estradiol concentrations coincided with maximum CaBP-9k mRNA expression at proestrus. Despite minimal concentrations of 17 beta-estradiol at estrus, CaBP-9k mRNA was still present at 10% of the proestrus level. At diestrus, CaBP-9k mRNA was not detectable despite increasing 17 beta-estradiol. It is concluded that CaBP-9k is subject to 17 beta-estradiol regulation during the estrous cycle. Correlation between CaBP-9k mRNA and 17 beta-estradiol levels indicates a lag period for CaBP-9k induction in diestrus following a rise in steroid hormone levels.

Animals↗
PubMed1993

In situ hybridization for creatine kinase-B messenger RNA in rat uterus and brain.

Creatine kinase-B (CKB) is present in both uterus and brain, and in uterus its synthesis (protein and mRNA) is regulated by estrogen. In the present study we have used in situ hybridization to detect CKB mRNA in uterus and brain, and to determine whether there is cell type specific induction of CKB by estrogen in these tissues. Tissue was taken from ovariectomized (ovx) rats that had been injected with either estrogen (17 beta-estradiol-3-benzoate and/or 17 beta-estradiol) or vehicle alone, 2, 8, 24 and 72 h previously. The brains and uteri were removed, frozen, cryostat-sectioned, and processed for in situ hybridization histochemistry. The uterine and brain sections were incubated with a tritiated DNA probe complementary to a 3' fragment of CKB mRNA, or a control sense probe to the same 3' fragment. In uterine smooth muscle cells, a 2.5- and 3.5-fold induction of CKB mRNA was observed 2 and 24 h after estrogen administration, respectively, and levels approached ovx controls at 72 h. A smaller induction (1.9-fold, 2 h) was observed in uterine epithelium, with little induction of CKB mRNA in stroma. In the brain CKB mRNA was detected in neurons, but not in clearly identified glia, and only occasionally in ependymal cells. In brain regions containing estrogen receptors there was no evidence of a significant estrogen effect on CKB mRNA levels. Some brain regions had higher neuronal expression than others (e.g. medial septum vs. preoptic area), but expression was widespread and not limited to neuroendocrine sites.

Animals↗
PubMed1995

Effects of retinoic acid and estrogens on oxytocin gene expression in the rat uterus: in vitro and in vivo studies.

We and others have previously identified functional estrogen (E) and retinoic acid (RA) response elements in the human and rat oxytocin (OT) gene promoters. Whereas there is no direct evidence for a significant role of E or RA in the regulation of rat hypothalamic OT gene expression, we have recently demonstrated that in vivo administration of E strongly stimulates uterine OT gene expression. Here, we show that in vivo administration of RA similarly induces a significant increase in uterine OT gene expression. Moreover, we report that the E and RA effects are reproducible in vitro. Using short-term uterine organ explant cultures derived from 18-day pregnant rats, we found that E (50 nM) and RA (0.4 nM) increased OT mRNA levels 5.2- and 3-fold, respectively, suggesting a direct action of these agents on uterine OT gene expression. Finally, we analyzed uterine E and RA receptor gene expression during pregnancy. Using semi-quantitative Northern blot analysis, we found that mRNAs encoding the E receptor, the RA receptor alpha and RA receptor beta are present in rat uterus and that their levels rise by 3.7-, 3.6- and 5.8-fold, respectively, between day 14 of gestation and term. Taken together, the data suggest that, at term, the rat uterus has an increased capacity to respond to E and RA, and that both agents may be involved in mediating the dramatic increase of OT mRNA accumulation observed in the uterus at term.

Animals↗
PubMed1988

Influence of mouse uterus on the metastatic patterns of tumour cells.

Metastatic patterns of fibrosarcoma (FS) and Lewis lung carcinoma (LLC) cells transplanted into mouse uteri of various reproductive stages, were investigated. Tumour cells were infused non-surgically into the lumen of 3-day post coitum pregnant uterus or into non-pregnant uterus of known estrus stage. The fate of these tumour cells was studied histologically on days 2, 5 and 10 post treatment. No significant difference in the metastatic patterns of the FS or the LLC cells was seen between the non-pregnant uteri of various estrus stages. FS cells in few cases of non-pregnant uteri displayed the tendency to migrate and grow outside the myometrium without colonizing in the endometrium, but in pregnant uteri they colonized within the endometrium. LLC cells in the non-pregnant uteri promptly metastasized to distant organs like liver and lung; but those in the pregnant uteri rarely metastasized to other organs. These observations imply that the metastatic patterns of uterine tumour might depend on both the physiological state of the uterus and the tumour cell type.

Animals↗
PubMed1984

Demonstration of paracervical ganglion origin for the vasoactive intestinal peptide-containing nerves of the rat uterus using retrograde tracing techniques combined with immunocytochemistry and denervation procedures.

The origin of the abundant vasoactive intestinal peptide (VIP)-immunoreactive nerves in the uterus has not been fully determined. In this study, a fluorescent dye, True Blue was injected into the uterus of rat and 6 days later, neuronal cell bodies of the paracervical ganglion were found to be labelled by this dye. Some of these labelled ganglion cells were also found to contain VIP immunoreactivity by immunocytochemistry. When the preganglionic pelvic and/or hypogastric nerves of rats were sectioned, the VIP-immunoreactive nerves in the uteri were not depleted, indicating that these nerves did not originate from the splanchnic ganglion, dorsal root ganglion or the spinal cord. Therefore it is concluded that VIP-immunoreactive nerves in the uterus originate from the paracervical ganglion.

Animals↗