Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “UTERUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed2003

Expression and regulation of cytosolic prostaglandin E synthase in mouse uterus during the peri-implantation period.

Prostaglandin E(2) (PGE(2)) is considered important for blastocyst spacing, implantation, and decidualization in rodent uteri. PGE synthase (PGES) catalyzes the isomerization of PGH(2) to PGE(2). Two isoforms of PGES exist: microsomal PGES (mPGES) and cytosolic PGES (cPGES); however, the expression and regulation of cPGES in the mammalian uterus during early pregnancy are still unknown. The aim of this study was to investigate the differential expression of cPGES in mouse uterus during early pregnancy and its regulation under different conditions using in situ hybridization and immunohistochemistry. A strong level of cPGES mRNA signal was exhibited in the stromal cells at the implantation site on Day 5 of pregnancy, whereas cPGES immunostaining was strongly detected in the luminal epithelium. The signals for both cPGES mRNA and immunostaining were strongly detected in the decidualized cells from Days 6-8 of pregnancy. A basal level of cPGES mRNA signal and immunostaining was exhibited in the uterus in delayed implantation. After delayed implantation was terminated by estrogen treatment and embryo implantation was initiated, cPGES mRNA signal was strongly detected in the stroma underlying the luminal epithelium at the implantation site, and cPGES immunostaining was strongly observed in the luminal epithelium surrounding the implanting blastocyst. A strong cPGES mRNA signal and immunostaining were detected in decidualized cells under artificial decidualization, whereas only a basal level of cPGES mRNA signal and immunostaining were observed in the control horn. Our data suggest that cPGES may play an important role during implantation and decidualization.

Animals↗
PubMed2003

Attenuation of estrogenic effects by dihydrotestosterone in the pig uterus is associated with downregulation of the estrogen receptors.

Androgens are known to attenuate some effects of estradiol-17beta (E) in the uterus. The objectives of the present experiment were to determine effects of 5alpha-dihydrotestosterone (DHT) on estrogenic actions in the pig uterus and its associations with changes in expression of the estrogen receptor (ER) alpha and ERbeta. Postpubertal gilts (120-130 kg of body weight; n = 16) were ovariectomized, and 3-4 weeks later received once-a-day injections (i.m.) of one of the following treatments during four consecutive days: 1) vehicle (corn oil), 2) E (250 microg), 3) E (250 microg) plus 1 mg DHT, or 4) E (250 microg) plus 10 mg DHT. Uterine tissues were collected 24 h after the last treatment. Gilts receiving E or E plus 1 mg DHT had greater uterine wet weight, uterine horn diameter, luminal epithelium thickness, and endometrial gland diameter compared with gilts treated with vehicle or E plus 10 mg DHT. Gilts receiving E or E plus 1 mg DHT were not different in these characteristics. Relative amounts of mRNAs in the endometrium for the cell proliferation marker histone H2a and the E-inducible protein complement component C3 increased in gilts treated with E compared with gilts treated with vehicle. E-induced increases in histone H2a and C3 mRNAs were not altered by cotreatment with E plus 1 mg DHT but were inhibited by E plus 10 mg DHT. Androgen receptor (AR) mRNA in the endometrium increased by treatment with E. Cotreatment of gilts with E and DHT did not alter the E-induced AR mRNA increase. Gilts treated with E plus 10 mg DHT had lesser amounts of immunoreactive ERalpha in cell nuclei of the myometrium and endometrial stroma and a tendency for a decrease in luminal epithelium compared with gilts treated with E. Amounts of immunoreactive ERalpha in glandular epithelium were not influenced by the treatments. Relative amounts of ERalpha and ERbeta mRNAs decreased in the endometrium of gilts treated with E plus 10 mg DHT compared with gilts treated with E. Downregulation of the ERs, particularly ERalpha in the myometrium and endometrial stroma, might be a relevant mechanism in the antagonism of estrogenic effects by DHT in the pig uterus.

Androgens↗
PubMed2003

Differential expression of ezrin/radixin/moesin (ERM) and ERM-associated adhesion molecules in the blastocyst and uterus suggests their functions during implantation.

Development of the blastocyst to implantation competency, differentiation of the uterus to the receptive state, and a cross talk between the implantation-competent blastocyst and the uterine luminal epithelium are all essential to the process of implantation. In the present investigation, we examined the possibility for a potential cross talk between the blastocyst and uterus involving the ezrin/radixin/moesin (ERM) proteins and ERM-associated cytoskeletal cross-linker proteins CD43, CD44, ICAM-1, and ICAM-2. In normal Day 4 blastocysts and after rendering dormant blastocysts to implantation-competent by estrogen in vivo (activated), the outer surface of mural trophectoderm cells showed much higher levels of radixin as compared to those in the polar trophectoderm cells, inner cell mass (ICM), and primitive endoderm. In contrast, ezrin was present on both the mural and the polar trophectoderm cell surfaces of normal Day 4 and activated blastocysts at higher intensity than dormant blastocysts. A distinct localization was noted in the primitive endoderm of dormant blastocysts that was not apparent in activated or normal Day 4 blastocysts. The expression of moesin was modestly higher at the mural trophectoderm of implantation-competent blastocysts, while the localization appeared to be present primarily on the polar trophectoderm cell surface of Day 4 blastocysts. The localization of ERM-associated adhesion molecules CD43, CD44, and ICAM-2 was more intense in the implantation-competent blastocysts compared with the dormant blastocysts. However, while CD44 was present both in the trophectoderm and in ICM, CD43 and ICAM-2 were localized primarily to the trophectoderm. The signal for ICAM-1 was very intense in the ICM but was modest in the trophectoderm. No significant changes in fluorescence intensity were noted between activated and dormant blastocysts. In the receptive uterus on Day 4 of pregnancy, ERM proteins were localized to the uterine epithelium, while on Day 5 the localization, especially of radixin and moesin, extended to the stroma surrounding the implantation chamber. With respect to ERM-associated adhesion molecules, while CD44 and ICAM-1 were exclusively localized in the stroma on Day 4, CD43 and ICAM-2 were localized to the epithelium. On Day 5, the localization of CD44 and ICAM-1 became highly concentrated in the antimesometrial stroma of the implantation chamber. The localization of CD43 and ICAM-2 remained mostly epithelial, although some stromal localization of CD43 was noted on Day 5. These results suggest that differential expression and distribution of ERM proteins and ERM-associated adhesion molecules are involved in the construction of the cellular architecture necessary for blastocyst activation and uterine receptivity leading to successful implantation.

Animals↗
PubMed2004

Estrogen induces expression of secretory leukocyte protease inhibitor in rat uterus.

In rodents, the steroid hormone estrogen (E) profoundly influences the early events in the uterus leading to embryo implantation. It is thought that E triggers the expression of a unique set of genes in the endometrium that in turn control implantation. To identify these E-induced genes, we employed a delayed implantation model system in which embryo attachment to rat endometrium is dependent upon E administration. Using a gene expression screen method, we isolated a number of cDNAs representing mRNAs whose expression is either turned on or turned off in response to an implantation-inducing dose of E. We identified one of these cDNAs as that encoding secretory leukocyte protease inhibitor (SLPI), an inhibitor of serine proteases. The expression of SLPI mRNA was induced in the uteri of ovariectomized rats in response to E, confirming the hormonal regulation of this molecule. Spatiotemporal analysis revealed a biphasic pattern of expression of SLPI mRNA during early pregnancy. A considerable amount of SLPI mRNA was detected in the uterine epithelium on Day 1 of pregnancy. The level of this mRNA, however, declined sharply on Days 2 and 3 of gestation. Interestingly, on Day 4 of gestation, there was a marked resurgence in SLPI mRNA expression in the uterine epithelium. This second burst of SLPI expression diminished by Day 6 of pregnancy. The transient induction of SLPI mRNA during Days 4 and 5 overlapped with the window of implantation in the rat. Although the precise function of SLPI in the uterus eludes us presently, its known effects as a serine protease inhibitor in other tissues and its hormone-induced expression in the rat uterus immediately preceding implantation lead us to propose that this gene plays an important role in controlling excessive proteolysis and inflammation during a critical phase of early pregnancy.

Animals↗
PubMed2006

WNT pathways in the neonatal ovine uterus: potential specification of endometrial gland morphogenesis by SFRP2.

Endometrial glands are critical for uterine function and develop between birth (Postnatal Day [P] 0) and P56 in the neonatal ewe. Endometrial gland morphogenesis or adenogenesis involves the site-specific budding differentiation of the glandular epithelium from the luminal epithelium followed by their coiling/branching development within the stroma of the intercaruncular areas of the endometrium. To determine whether WNT signaling regulates endometrial adenogenesis, the WNT signaling system was studied in the neonatal ovine uterus. WNT5A, WNT7A, and WNT11 were expressed in the uterine epithelia, whereas WNT2B was in the stroma. The WNT receptors FZD2 and FZD6 and coreceptor LRP6 were detected in all uterine cells, and FZD6 was particularly abundant in the endometrial epithelia. Secreted FZD-related protein-2 (SFRP2), a WNT antagonist, was not detected in the P0 uterus, but was abundant in the aglandular caruncular areas of the endometrium between P7 and P56. Exposure of ewes to estrogens during critical developmental periods inhibits or retards endometrial adenogenesis. Estrogen-induced disruption of endometrial adenogenesis was associated with reduction or ablation of WNT2B, WNT7A, and WNT11, and with an increase in WNT2 and SFRP2 mRNA, depending on exposure period. Collectively, results implicate the canonical and noncanonical WNT pathways in regulation of postnatal ovine uterine development and endometrial adenogenesis. Expression of SFRP2 in aglandular caruncular areas may inhibit the WNT signaling pathway, thereby concentrating WNT signaling and restricting endometrial adenogenesis in the intercaruncular areas of the uterus. Further, estrogen-induced inhibition of adenogenesis may be mediated by a reduction in WNT signaling caused by aberrant induction of SFRP2 and loss of several critical WNTs.

Animals↗
PubMed2006

Selectin, platelet plays a critical role in granulocyte access to the pregnant mouse uterus under physiological and pathological conditions.

Leukocyte recruitment to the pregnant mouse uterus is associated with highly regulated patterns of expression of vascular adhesion receptors. One striking observation is the localized expression of mucosal vascular addressin cell adhesion molecule (MADCAM1) and selectin, platelet (SELP, formerly P-selectin) by maternal vessels in the vascular zone (VZ) during the first half of pregnancy. From midgestation onwards, endothelial cells lining the maternal vessels of the VZ in addition express vascular cell adhesion molecule-1 (VCAM1). The predominant cell population within these vessels is monocyte-like cells. Granulocytes and low numbers of lymphocytes are also present. Murine fetal trophoblast cells are almost devoid of adhesion molecules, including SELP. In contrast, spontaneous abortions of allogeneic pregnancies are characterized by dramatic upregulation of SELP on maternal VZ vessels and on fetal trophoblast cells. Upregulation of SELP is associated with a dramatic influx of highly activated granulocytes, which infiltrate the vessels and tissue of the VZ and the trophoblast. The majority of the activated granulocytes within the trophoblast undergo nuclear fragmentation, which can be detected by TUNEL staining. To demonstrate that SELP is involved in the recruitment of granulocytes to the pregnant uterus, we undertook long-term in vivo inhibition studies using a monoclonal antibody to inhibit the contribution of SELP to leukocyte trafficking to the decidua. In addition, the pregnant uteri of syngeneic Selp(-/-) x Selp(-/-) mice were investigated and compared to the controls. Our results clearly demonstrate the importance of SELP for granulocyte access to the pregnant mouse uterus under physiological and pathological conditions.

Abortion, Veterinary↗
PubMed1982

Surface changes in oviduct, uterus and vaginal cells of neonatal mice after estradiol-17 beta and the insecticide chlordecone (Kepone) treatment: a scanning electron microscopic study.

Surface changes in cells lining the oviduct, uterus and vagina of a neonatal mouse were studied after treatment with estradiol-17 beta (E2) or the insecticide chlordecone. One-day-old mice received daily intraperitoneal injections of 1 of 6 injection mixtures (0.05 ml) for 10 days. The daily dosages per animal were as follows: sesame oil only, 10 microgram E2, 15, 30, 60 and 125 microgram chlordecone suspended in sesame oil. Estradiol-treated mice were terminated after 5 and 10 injections, whereas all other mice were terminated at the end of 10 injections. After 5 and 10 estradiol injections, accelerated ciliation was recorded in the oviduct and increased secretory activity in the uterus or uterine glands. In the vagina, epithelial mucification proceeded to complete cornification with the cornified cell surfaces showing a prominent and complex pattern of microridges. Chlordecone treatments produced dose-dependent cell surface changes in the reproductive tract that were either characteristic of estrogenic stimulation or atypical responses. Chlordecone stimulatory action mimicked estrogen in the form of accelerated ciliation, secretory activity in oviductal and uterine cells as well as mucification leading to complete cornification of vaginal epithelium. Chlordecone doses of 60 microgram or higher produced atypical cellular expansions or swelling in the nonciliated cells of the oviduct and uterus in the mucified vaginal epithelial cells. Also, cornified vaginal cells of chlordecone-treated mice exhibited smoother cell surfaces with decreased microridge patterns when compared to estradiol-treated mice. The stimulatory mechanism of chlordecone action and the probable cause of cellular abnormality are discussed in the text.

Animals↗
PubMed1982

Deciduoma formation in uterus of genetically mast cell-deficient W/Wv mice.

The role of mast cells in deciduoma formation in the uterus of mice was investigated by using genetically mast cell-deficient (WB x C57BL/6)F1-W/Wv (hereafter called WBB6F1-W/Wv) mice. Deciduoma formation occurred in castrated WBB6F1-W/Wv mice after estradiol-progesterone injection and traumatization in spite of their deficiency of mast cells. Injection of diphenhydramine, which blocks histamine receptors, inhibited deciduoma formation in WBB6F1-W/Wv mice as well as in congenic +/+ mice. THe uterus of WBB6F1-W/Wv mice contained about 10% of the amount of histamine found in the uterus of +/+ mice. These results suggest that mast cells are not essential for formation of deciduomata and that histamine originating from sources other than mast cells may be important in deciduoma formation.

Animals↗
PubMed1988

Immunohistochemical localization of prostaglandin synthase in the rat uterus and embryo during the peri-implantation period.

Prostaglandins (PGs) appear to have a role in the appearance of the increased uterine vascular permeability and subsequent decidualization observed at implantation in many species. However, the sites of production of these PGs have not been clearly established. To clarify the PG synthetic capacity of the blastocyst and the various types of cells in the uterus at implantation, we have studied the immunohistochemical localization of PG synthase in the rat blastocyst on Days 5 to 7 and uterus on Days 1, 4, 5, 6, and 7 of pregnancy. Labeling of PG synthase was negligible in the uterus on Day 1 of pregnancy. On Day 4, there was increased labeling in the luminal and glandular epithelium, in stromal cells adjacent to the luminal epithelium, and in blood vessels and some leukocytes. PG synthase was detected in the blastocysts on Days 5 to 7, but there was a gradual loss of label in the luminal and glandular epithelial cells during this period. Early differentiating stromal cells adjacent to the luminal epithelium in the implantation site on Day 5 showed bright labeling, whereas peripheral stromal cells were only slightly labeled. By Day 7, the differentiated cells of the primary decidual zone showed little or no label, but cells in the secondary decidual zone were brightly labeled. These results indicate that PG synthase is present in the rat blastocyst and in several kinds of uterine cells, and that its localization in uterine cells changed markedly during the implantation process.

Animals↗
PubMed1991

Ontogeny of the production of an estrogen-regulated eosinophil chemotactic factor in the rat uterus.

The ontogeny of an estrogen-induced eosinophil chemotactic activity in the uterus after estrogen administration and its regulation by progesterone was studied in neonatal rats at 3, 7, 10, and 13 days of age. These results were compared with the increase in peroxidase activity and the secretion of complement component C3 by the uterus. No chemotactic activity was observed in animals younger than 14 days, and after this age the estrogen regulation of the response was also prevented by the co-administration of progesterone. The secretion of complement C3 appeared earlier, at 10 days of age. It was also observed that the uterus of 3-7-day-old rats responded to estrogen by increasing the secretion of two proteins of 36 and 110 kDa. No further regulation or synthesis was observed with increasing age for these two proteins.

Aging↗
PubMed1992

The expression of thromboxane A2 synthase and thromboxane A2 receptor gene in human uterus.

The expression of thromboxane (TX) A2 synthase and thromboxane A2 receptor gene in human uterus was investigated by immunoblotting, immunocytochemistry, Northern blot, in situ hybridization, and autoradiographic analyses. Human uterus contains a single immunoreactive protein of 55 kDa that corresponds to the molecular size of human TXA2 synthase. Human uterus also contains a single 2.8-kb TXA2 receptor mRNA transcript and a receptor protein that can bind TXA2 antagonist, 125I-PTA-OH. The immunoreactive TXA2 synthase, TXA2 receptor mRNA, and protein are present in endometrial glands, stromal cells, myometrial smooth muscle, and uterine blood vessels. The TXA2 synthase and TXA2 receptors in different uterine cells varied within as well as between various reproductive states. There were differences in the binding site numbers even between elongated and circular myometrial smooth muscle in all reproductive states except postmenopause. In summary, the data presented demonstrate for the first time that different human endometrial and myometrial cells and uterine blood vessels express TXA2 synthase as well as TXA2 receptor gene. The expression, as well as changes during various reproductive states, suggests that TXA2 could be an autocrine/paracrine regulator of human myometrial contractions, endometrial secretory functions, and intrauterine blood flow and could play a role in the initiation and/or progression of labor in women.

Autoradiography↗
PubMed1994

Distribution of transforming growth factor alpha precursors in the mouse uterus during the periimplantation period and after steroid hormone treatments.

Temporal and cell-type specific distribution of transforming growth factor alpha (TGF alpha) precursor (proTGF alpha) was examined in the mouse uterus during the periimplantation period, and after steroid hormone treatments of ovariectomized adult mice by immunohistochemistry using antibodies that recognize the precursor forms of the growth factor. These studies were complemented by immunoblot analysis of proTGF alpha in separated uterine cell-type preparations. The specificity of the antibodies used in these studies was confirmed by use of pancreas or lactating mammary glands from transgenic mice in which mutated proTGF alpha, lacking recognition sites for proteolytic cleavages, was targeted for expression under a tissue-specific enhancer/promoter. Analysis of histochemical studies revealed accumulation of immunoreactive proTGF alpha primarily in luminal and glandular epithelial cells on Day 1 of pregnancy or pseudopregnancy followed by little or no accumulation on Days 2 and 3. However, immunoreactive proTGF alpha started to reappear in the luminal epithelium on the morning of Day 4 and became more prominent in the afternoon. In pregnant mice, immunostaining persisted in these cells at the implantation sites during the time of attachment reaction (2130 h on Day 4), but disappeared by morning of Day 5. Immunostaining appeared to be situated at the apical border of the luminal epithelium. No positive immunostaining could be detected in the nonreceptive uterus on Day 5 or 6 of pseudopregnancy. Consistent with the immunohistochemistry results, Western blot analysis detected two species of precursor proteins (14.5 and 17 kDa) in isolated luminal epithelial cell-enriched preparations on Day 4, but not on Day 5, of pseudopregnancy. The results suggest that proTGF alpha accumulates in the luminal epithelium of the receptive uterus prior to implantation. The effects of ovarian steroids on uterine accumulation of proTGF alpha were examined in ovariectomized adult mice by immunohistochemistry and immunoblotting. Whereas an injection of estradiol-17 beta (E2) or progesterone (P4) had little or a modest effect on epithelial accumulation of proTGF alpha, P4 priming for several days resulted in distinct accumulation of proTGF alpha in epithelial cells. The superimposition of an E2 treatment on P4 priming showed a biphasic response, with an initial gradual loss of immunostaining through 12 h followed by a return by 24 h of E2 treatment. The combined hormone treatment schedule employed here is similar to the situation of inducing implantation with E2 in P4-primed delayed implanting mice. The results suggest a paracrine/"juxtacrine" role for this growth factor in implantation.

Animals↗
PubMed1994

CaBP9K levels during the luteal and follicular phases of the estrous cycle in the bovine uterus.

The expression of calbindin-D9K (CaBP9K) and calbindin-D28K (CaBP28K) genes in the reproductive system is well established for rodent and avian species, but not for domestic livestock. This investigation expanded the study of these proteins to include the bovine uterus and examined the levels of CaBP9K and CaBP9K mRNA in the nonpregnant bovine uterus during the estrous cycle. Immunohistochemical studies revealed that CaBP9K was present in all uterine glandular and luminal epithelial cells. In contrast, the closely related calcium binding protein CaBP28K was present in only one to two glandular cells in the samples examined. Neither protein was localized in the myometrium or in the stromal cells of the endometrium. RIA and dot blot hybridization were used to quantify the amount of CaBP9K and CaBP9K mRNA. The levels of both the protein and its mRNA were threefold higher during the luteal phase than during the follicular phase. RIA was also used to determine bovine uterine levels of 17 beta-estradiol and progesterone. Progesterone levels were higher during the luteal phase than during the follicular phase, while 17 beta-estradiol levels were higher during the follicular phase. This investigation represents the first characterization of CaBP9K gene expression in the bovine uterus. It demonstrated that the expression of CaBP9K and CaBP9K mRNA was greatest during the progesterone-dominated luteal phase of the bovine estrous cycle. These results indicated that CaBP9K may be involved in uterine glandular function during the luteal phase.

Animals↗
PubMed1995

Expression of SQ10 (a preprorelaxin-like gene) in the pregnant rabbit placenta and uterus.

A Northern blot containing poly(A)+ RNA isolated from pregnant rabbit placenta, uterus, ovary, mammary gland, psoas muscle, and intestine was hybridized with an oligonucleotide probe to porcine preprorelaxin. Only the placenta and uterus exhibited high levels of a 1-kb mRNA that hybridized to the probe. Porcine preprorelaxin primers were used to generate and amplify cDNAs from placental and uterine poly(A)+ RNA. Southern blot analysis of the placental and uterine cDNAs each revealed a single PCR product that hybridized with the porcine relaxin probe. The sequence of the cDNAs exhibited 100% identity with SQ10, a preprorelaxin-like gene identified in rabbit tracheobronchial epithelial cells. Identical results were obtained with primers specific for SQ10. SQ10 is expressed in tracheobronchial epithelial cells during abnormal conditions, such as mechanical or toxic injury. The protein is believed to have a role in tracheal epithelial cell differentiation and transformation that occurs under the above conditions. This work shows, for the first time, the presence of high levels of message for SQ10 in normal reproductive tissues. The expression of SQ10 in the uterus and placenta may suggest an important role in cell differentiation and transformation that occurs in these tissues during pregnancy.

Amino Acid Sequence↗
PubMed1995

Cellular pattern of c-fos induction by estradiol in the immature rat uterus.

Previous biochemical studies have shown that c-fos mRNA expression is rapidly and dramatically induced by estrogen in the immature rat uterus. In this work we have used in situ hybridization and immunocytochemistry to analyze the cellular pattern of proto-oncogene induction following administration of estradiol. The c-fos transcript and protein levels were low in control animals. Three hours after hormone treatment, the luminal and glandular epithelium, stroma, and myometrium all showed a clear increase in mRNA levels of the proto-oncogene as judged by in situ hybridization; this increase was most pronounced in the epithelial cells. Immunocytochemistry also demonstrated Fos expression in all cell layers with a higher fraction of cells staining in the epithelial and stromal layers than in the myometrium. Estradiol thus increased expression of c-fos in all major cell types of the immature uterus, although each tissue layer exhibited a specific pattern and degree of fos transcript and protein expression. This proto-oncogene is thus a marker for estrogen action in all uterine cell types at this stage of development. Since estrogen stimulates proliferation in all cell layers of the immature uterus, the cellular pattern of fos expression also correlates with the proliferative response to the hormone.

Animals↗
PubMed1996

Ontogeny of estrogen receptor messenger ribonucleic acid expression in the postnatal rat uterus.

During the first 2 wk of postnatal life, the rodent uterus undergoes a period of marked growth and differentiation. To further examine the role of the estrogen receptor (ER) in the mediation of uterine development, we analyzed the ontogeny of ER mRNA expression in the postnatal rat uterus using in situ hybridization. ER mRNA was present in the uterine stroma on the day of birth and progressively increased in abundance during the first 2 wk of postnatal life. In contrast, ER mRNA was not detectable in the luminal epithelium at birth and did not become abundant in this region until postnatal day (P) 7. ER mRNA abundance increased in the luminal epithelium and in the invaginating and fully formed glandular epithelium during the second week of life. At P21 ER mRNA was more abundant in the glandular epithelium than in any other uterine cell type. These results are consistent with, and extend the findings of, previous studies using uterine homogenate binding assays and immunohistochemistry to define ER ontogeny in rodents. Delineation of the temporal and cell-type specific pattern of ER mRNA ontogeny in the postnatal rat uterus furthers our understanding of the molecular basis of both endogenous and exogenous estrogen effects on uterine growth and development.

Aging↗
PubMed1997

Changes in the expression of adenylyl cyclases in the rat uterus during the course of pregnancy.

The changes in the expression of the various adenylyl cyclases (ACs) in the rat uterus during the course of pregnancy and after delivery were examined by Northern blot analysis and AC assay. Northern blot analysis revealed that five isoforms of ACs (AC2, AC4, AC6, AC7, and AC9) were expressed in the rat uterus, AC6 being the most abundant. The level of expression of these ACs increased 1.7- to 3.4-fold during the course of pregnancy and diminished near term and after delivery. The highest level of expression in each type of AC was consistently seen on Day 17 of pregnancy, and the relative increase of expression, as compared to that in nonpregnant rats, was as follows: AC2 > AC4 > AC7 > AC9 > AC6. In agreement with these findings, both basal and forskolin-stimulated AC activities exhibited a 2- to 3-fold increase during the course of pregnancy, followed by a decrease near term. Our data indicate that post-receptor events, namely marked changes in the level of AC mRNA (and presumably proteins) occur during pregnancy and after delivery and that they contribute to the essential role of cAMP in maintaining uterus quiescence.

Adenylyl Cyclases↗
PubMed1997

Thioredoxin messenger ribonucleic acid is regulated by estradiol in the rat uterus.

Thioredoxin is a major cellular dithiol reductant with a large number of functions in electron transport and thiol redox control of enzymes and transcription factors. To investigate the expression and regulation of thioredoxin in the uterus, 35 rats were ovariectomized (OVX) and treated 14 days after surgery with either growth hormone (GH), dexamethasone (DEX), or estradiol (E2), or combinations of these, for 24 h. Thioredoxin mRNA levels were determined by solution hybridization. The animals receiving E2 or a combination of E2 and DEX showed significantly increased thioredoxin mRNA levels, by 4-fold and 5-fold, respectively, as compared to the OVX control group. The GH or GH+DEX-treated groups did not display any difference in thioredoxin mRNA levels. Thioredoxin mRNA was also measured at different time points in uteri from OVX rats treated with daily E2 injections and was found to be transiently increased, with a maximum 48 h after the initiation of the E2 treatment. In contrast, the thioredoxin mRNA level in the liver of OVX rats was about 10-fold higher than in the uterus but remained unaffected by the different hormone treatments. We conclude that thioredoxin mRNA is expressed in the rat uterus, and up-regulated by E2 in a tissue-specific manner, with a maximum at 48 h after the initiation of hormone treatment.

Animals↗