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At least 19 recordsLinked to original sources
PubMed1988

The significance of prostacyclin produced by pregnant rat myometrium: the relationship between myometrial prostacyclin producing activity and passive stretch of myometrium by growing conceptus.

The present experiment was performed to elucidate the significance of prostacyclin (PGI2) produced by pregnant rat myometrium. PGI2-like substance producing activity of various portions of the uterus was measured at selected gestational stages by platelet bioassay; surface area per 1 gm of uterine wall enveloping one conceptus was calculated; and spontaneous contractility of myometrium of both conceptus and non-conceptus regions and the effects of authentic PGI2 on it were examined. PGI2-like substance producing activity increased with advancing pregnancy, but the activity varied according to area of the myometrium, being highest in the area where it was most greatly stretched by the growing conceptus and lowest where no conceptus was contained. Spontaneous contractility was reduced in regions with high PGI2 producing activity. Though authentic PGI2 generally exhibited a stimulatory effect, it had an inhibitory effect on Day 10 pregnant myometrium. From these results, it may be concluded that the producing activity of PGI2, which remarkably increases in the conceptus region with the advance of pregnancy, keeps the uterine wall relaxed, making the uterus adapt to the growth of the fetus. Passive myometrial stretch by the growing conceptus is thought to be one of factors which enhance myometrial PGI2 producing activity.

Animals↗
PubMed2003

Inhibition of rho-associated kinase reduces MLC20 phosphorylation and contractility of intact myometrium and attenuates agonist-induced Ca2+ sensitization of force of permeabilized rat myometrium.

The role of rhoA/rho-associated kinase (ROK) signaling pathways in agonist-induced contraction of the rat myometrium was investigated. We measured the [Ca(2+)](i)-force relationship, phosphorylation of myosin regulatory light chains (MLC(20)) in intact tissue and the Ca(2+)-sensitization of force in permeabilized myometrial cells of rat. In measurements of the relationship between [Ca(2+)](i) and tension in intact tissue, Y-27632, a ROK inhibitor, significantly attenuated the carbachol-induced contraction without changing [Ca (2+)](i). Phosphorylation of MLC(20) was increased by carbachol and this increased phosphorylation was blocked by treatment of tissue with Y-27632. In tension measurements of single hyperpermeable cells, carbachol evoked sustained contraction at constant pCa 6.7 and these agonist-induced contractions were decreased by treatment with Y-27632. These results suggest that activation of a ROK-mediated signaling pathway(s) plays an important role in agonist-induced alterations in MLC(20) phosphorylation and force of rat myometrium.

Amides↗
PubMed1998

Mechanisms of galanin-induced contraction in the rat myometrium.

A neuropeptide, galanin, regulates the reproductive process and directly induces myometrial contraction. The aim of this study was to determine the mechanism of galanin-induced myometrial contraction. For this purpose, we simultaneously measured intracellular Ca2+ concentration ([Ca2+]i) and tension using fura-PE3-fluorometry and the rat longitudinal myometrium. The effect of galanin on the Ca2+ sensitivity of the contractile apparatus was examined in beta-escin permeabilized strips. The expression of galanin and the galanin receptors mRNAs in the rat myometrium were determined by reverse transcription polymerase chain reaction (RT-PCR). Galanin (10-300 nM) induced phasic contraction with or without oscillation in the pregnant rat myometrium in a concentration-dependent manner. The maximal response was obtained at 100 nM. There was no significant difference either in the maximal responses or EC50 values for galanin-induced myometrial contractions among myometriums from non-pregnant and pregnant (day 4, day 11, day 20, day 22) rats. In the day 20 and 22 pregnant myometriums, assigning the levels of [Ca2+]i and tension at 40 mM K+-depolarization to be 100%, galanin increased the [Ca2+]i and tension to 126.9+/-2.9% and 116.3+/-2.7%, respectively. Diltiazem (10 microM) inhibited the galanin-induced elevation of [Ca2+]i and tension to 71.9+/-2.4% and 16.2+/-0.7%, respectively. Ni2+, by itself, decreased the basal [Ca2+]i to -50.2+/-3.9% without affecting resting tension. After Ni2+ treatment, galanin-induced increases in [Ca2+]i and tension were -19.6+/-3.4% and 0.9+/-0.1%, respectively. In myometrium treated with diltiazem, no oscillation in [Ca2+]i and tension was observed. In Ca2+-free solution with 0.1 mM EGTA, galanin increased [Ca2+]i from -40.2+/-2.7% to -18.0+/-2.6% and induced transient contraction (3.6+/-0.8%). In beta-escin permeabilized myometrium, galanin enhanced the contraction induced by 0.3 microM Ca2+ in the presence of GTP. In the presence of GDPbetaS (1 mM) instead of GTP, galanin failed to increase the Ca2+ sensitivity of the contractile apparatus. RT-PCR revealed that galanin mRNA was hardly expressed in the non-pregnant rat myometrium and increased to reach a maximal level at mid pregnancy (day 11), but decreased to the same level as in the non-pregnant myometrium at term (day 22). Type 2 galanin receptor (GALR2) mRNA was found to be expressed in the rat myometrium whereas type 1 galanin receptor (GALR1) mRNA expression was not detected. In conclusion, galanin induces contraction of the rat myometrium by increasing [Ca2+]i as well as by increasing Ca2+ sensitivity of the contractile apparatus. Galanin-induced increases in [Ca2+]i are caused by both intracellular Ca2+ release and Ca2+ influx from extracellular space. The responsiveness of the rat myometrium to galanin does not change during pregnancy. The galanin mRNA is expressed in the rat myometrium and it is upregulated during mid-pregnancy. Rat myometrium expresses GALR2 but not GALR1 mRNA. By changing mRNA expression in the myometrium during pregnancy, galanin may act as a paracrine or autocrine mediator in the regulation of myometrial contractility.

Animals↗
PubMed2003

Expression of estrogen receptor alpha and beta in myometrium of premenopausal and postmenopausal women.

Although a clear role for estrogen receptor (ER) alpha has been established, the contribution of ERbeta in estrogen-dependent development, growth and functions of the myometrium is not understood. As a first step towards understanding the role of ERbeta, we have examined the expression of ERalpha and ERbeta in the human myometrium. With competitive RT-PCR assays, the level of ERbeta mRNA was 10-200 times lower than that of ERalpha mRNA in both premenopausal and postmenopausal myometrium. In premenopausal myometrium, the expression pattern of ERbeta mRNA during the menstrual cycle was similar to that of ERalpha mRNA, with highest levels in peri-ovulatory phase. In postmenopausal myometrium, ERbeta mRNA was significantly higher than it was in premenopausal myometrium, while the level of ERalpha mRNA was lower. The net result was a change in the ratio of ERbeta to ERalpha mRNA expression. The ratio changed from 0.6-1.5 in premenopausal to 2.5-7.6 in postmenopausal myometrium. In premenopausal women, the gonadotropin releasing hormone analogue, leuprorelin acetate, elicited a decrease in ERalpha and an increase in ERbeta mRNA expression to cause a postmenopausal receptor phenotype. Estradiol, on the other hand, reversed ERalpha and ERbeta mRNA expression and their ratio in postmenopausal myometrium to those of premenopausal myometrium. Immunohistochemical staining and Western blot analysis of ERalpha and ERbeta with semiquantitative analysis showed good agreement between mRNA and protein levels. The data indicate that coordinated expression of ERalpha and ERbeta might be necessary for normal estrogen action in myometrium. Furthermore, estrogen appears a dominant regulator of both receptors in the myometrium.

Adult↗
PubMed2003

Possible role of the protein kinase C/CPI-17 pathway in the augmented contraction of human myometrium after gestation.

1. Activation of protein kinase C (PKC) by phorbol 12,13-dibutylate (PDBu, 1 microm) induced sustained contractions with no increase in [Ca2+]i in nonpregnant and pregnant human myometria. The contractile effects of PDBu in pregnant myometrium were much greater than those in nonpregnant myometrium, and the contractions in pregnant myometrium were accompanied by an increase in myosin light chain (MLC) phosphorylation at Ser19. 2. The contraction induced by PDBu in pregnant myometrium was inhibited by the inhibitors of conventional PKC isoforms, bisindolylmaleimides and indolocarbazole, such as Go6976, Go6983, and Go6850 (1 microM). LY333531 (1 microM), a specific inhibitor of PKC beta, also inhibited the PDBu-induced contraction in the pregnant myometrium. 3. In the pregnant myometrium permeabilized with alpha-toxin, PDBu increased the contractions induced at fixed Ca2+ concentration (0.3 microM) both in nonpregnant and pregnant myometria, indicating Ca2+ sensitization of contractile elements. 4. Western immunoblot analysis indicated that pregnant myometrium contained PKC isozymes such as conventional PKC (alpha, beta, gamma), novel PKC (delta, epsilon, theta), and atypical PKC (zeta but not iota and lambda). RT-PCR and real-time RT-PCR analysis indicated that, among the conventional PKC, the levels of mRNA of beta isoform in pregnant human myometrium were greater than those in nonpregnant myometrium. 5. CPI-17 is a substrate for PKC, and the phosphorylated CPI-17 is considered to inhibit myosin phosphatase. The levels of CPI-17 mRNA and protein expression were also greater in the pregnant myometrium. 6. These results suggest that the PKC-mediated contractile mechanism is augmented in human myometrium after gestation, and that this augmentation may be attributable to the increased activity of the beta PKC isoform and CPI-17.

Adult↗
PubMed2000

Gene expression and tissue concentrations of IGF-I in human myometrium and fibroids under different hormonal conditions.

The expression of insulin-like growth factor-I (IGF-I) was measured at the mRNA and protein level in myometrium and fibroids from women with and without preoperative treatment with a gonadotrophin-releasing hormone (GnRH) agonist for 3 months, from post-menopausal women, from pregnant women and in myometrium from women without fibroid disease. Women with menstrual periods were classified according to the phase of the cycle. In tissues from non-treated premenopausal women, IGF-I mRNA expression was significantly higher in fibroids than in myometrium, with no differences related to phase of the menstrual cycle. In post-menopausal women and in GnRH agonist-treated women responding to treatment, similar mRNA expression was seen in myometrium and fibroids but the concentrations were lower than in untreated premenopausal women. The IGF-I mRNA value in fibroids from pregnant women was higher than in any other group and myometrium from pregnant women exhibited higher mRNA expression than myometrium from non-treated premenopausal women. The IGF-I protein was more abundant in fibroids than in myometrium of non-treated premenopausal and of pregnant women and in both tissues the concentration was significantly higher in the group of pregnant women. The IGF-I protein concentrations in fibroids and myometrium from GnRH agonist-treated and post-menopausal women were similar to those from premenopausal non-treated women. High sex steroid concentrations in pregnant and non-pregnant women of fertile age seem to be associated with a higher expression of IGF-I in fibroids than in myometrium, suggesting that IGF-I contributes to the selective growth advantage of these tumours.

Adult↗
PubMed1996

Effects of glucocorticoids on estrogen receptor messenger ribonucleic acid in the pregnant ovine myometrium in vivo and in vitro.

We recently reported that estrogen receptor (ER) mRNA is dramatically increased in the sheep myometrium during cortisol-induced premature labor and term spontaneous labor. In this study, we compared myometrial ER mRNA and ER protein levels in tissues from pregnant sheep during infusions of two different glucocorticoids (dexamethasone and betamethasone). Tissues from glucocorticoid-infused sheep not yet in labor were compared with tissues from sheep in labor. The population of ER mRNA-containing cells in myometrium obtained from sheep in labor was determined by in situ hybridization and compared with that of sheep not in labor in order to understand how the cellular distribution of ER mRNA changed during labor. Finally, in vitro myometrial cell culture and immunolocalization of glucocorticoid receptor (GR) were used to determine 1) the effects of different steroids on ER mRNA content, 2) whether or not the myometrium is a functional site for glucocorticoid action, and 3) whether the change in ER mRNA content in the myometrium might be induced by glucocorticoid acting through GR. Increased ER mRNA and protein were found only in the myometrium associated with labor. In situ hybridization of ER mRNA and immunolocalization of ER protein showed that ER mRNA and protein were mainly located in the smooth muscle cells and endothelial cells of blood vessels. In vitro treatment of cultured myometrial cells with hydrocortisone resulted in a 3.5-fold increment in ER mRNA. In contrast, there was no obvious change in ER mRNA when myometrial cells were treated in vitro with either estradiol (10 nM) or progesterone (100 nM) for 24 h. GR was localized exclusively in the pregnant sheep myometrium. We conclude that 1) increased ER protein and ER mRNA in sheep myometrium are strongly associated with labor; 2) an increase in the population of ER-positive cells is associated with the increment of ER mRNA during glucocorticoid-induced labor; 3) in the pregnant sheep myometrium, both the smooth muscle cells and endothelial cells of blood vessels are positive for ER protein ER mRNA; and 4) hydrocortisone is a potent stimulus in vitro for increasing ER mRNA content, presumably acting through the GR present in the pregnant sheep myometrium.

Animals↗
PubMed2001

Activin betaA-subunit and activin receptors in human myometrium at term and during labour.

OBJECTIVE: To measure activin A content and to localise and semi-quantitate activin receptors in human myometrium at term and during labour. DESIGN: Myometrium was collected from non-pregnant women (n = 6), pregnant women at term not in labour (n = 6) and at term in labour (n = 6). SETTING: Monash Medical Centre, Melbourne, Australia. MAIN OUTCOME MEASURES: Tissue lysates of myometrium were analysed for activin A content using an enzyme-linked immunosorbent assay and activin receptor proteins IA, IIA and IIB using Western hybridisation. Activin betaA-subunit and activin receptors were localised in myometrium by immunohistochemistry. RESULTS: Activin A was detected by ELISA in non-pregnant, pregnant and labouring myometrium. Levels were significantly higher in labouring myometrium. The three activin receptors IA, IIA and IIB were detected in all myometrial samples by Western hybridisation. Receptor IA was expressed in significantly higher levels in pregnant myometrium. Receptor IIA was very weakly expressed throughout. The expression of receptor IIB was similar in all three groups. Activin betaA-subunit and all three receptors were localised to the endothelial cells of myometrial blood vessels. Neither activin betaA-subunit nor any of the three activin receptors were immunolocalised to myometrial smooth muscle cells in the three groups. This result was confirmed by Western blotting for expression of activin receptors in isolated myometrial smooth muscle and microvascular endothelial cells. CONCLUSION: The myometrium is not a target for activin A during late pregnancy or labour. However, activin A may have a role in the regulation of microvascular endothelial cell function in the myometrium.

Activin Receptors↗
PubMed2001

Activity and expression of soluble and particulate guanylate cyclases in myometrium from nonpregnant and pregnant women: down-regulation of soluble guanylate cyclase at term.

The role of cGMP in the regulation of human myometrial smooth muscle contractility is at present unclear. cGMP can be synthesized by a cytoplasmic, soluble guanylate cyclase (sGC), which is stimulated by nitric oxide and carbon monoxide, and by particulate membrane-bound GC, which are activated by natriuretic peptides. The aim of this study was to determine whether sGC or pGC are present in nonpregnant and pregnant human myometrium, and whether the activity and expression of these enzymes and the cGMP content change during pregnancy and with labor. Myometrium was obtained from nonpregnant women (n = 12) and pregnant women who were preterm (25-34 wk gestation; n = 12), term (>38 wk) not in labor (n = 14), or term in active labor (n = 12). The cGMP content in myometrium obtained from preterm deliveries was significantly higher than that in tissue obtained from nonpregnant women and decreased at term, especially in laboring groups. Protein and mRNA for sGC, particulate GC-A, GC-B, and the clearance receptor were detected in human myometrium. cGMP in pregnant human myometrium, however, appears to be produced predominantly by sGC and possibly by GC-B, as GC-A was only weakly expressed. sGC activity was greater in myometrium from preterm (nonlabor) deliveries compared those taken at term (in labor), but was down-regulated compared with activity in nonpregnant myometrium. Neither atrial natriuretic peptide nor C-type natriuretic peptide (agonists for GC-A and GC-B, respectively) altered contractility in vitro of myometrium from women at term (not in labor). We conclude that the cGMP/guanylate cyclase system in human myometrium is gestationally regulated and potentially plays an important role in mediating quiescence during early pregnancy. A reduction in cGMP availability may contribute to the switch to contractile activity at term.

Atrial Natriuretic Factor↗
PubMed2025

Transcriptomics and proteomics reveal associations between myometrium and intrauterine adhesions.

BACKGROUND: Intrauterine adhesions (IUAs) is a gynecological condition with a poor therapeutic prognosis, that severely threatens the fertility and the reproductive physiology and psychological health of women. Our previous research on the use of umbilical cord mesenchymal stem cells (HUCMSCs) for treating IUAs revealed that CM-Dil-labelled HUCMSCs were barely distributed in the endometrial epithelium. Instead, these cells were predominantly found in the myometrium, with no statistically significant difference in distribution compared to the endometrial stromal cells. Therefore, we aimed to explore the associations between the myometrium and IUAs. METHODS: Eight patients with moderate and 5 severe lesional IUAs were included in the experimental group. The control group included 7 patients whose inner and outer myometrium were normal. We used H&E, Masson's trichrome and immunohistochemical staining to obtain the pathological features of the tissues. Transcriptomic and proteomic analyses were conducted to identify differentially expressed genes, proteins and enrichment pathways. RESULTS: Both IUAs lesion tissues expressed the smooth muscle markers &#x3b1;-SMA and H-caldesmon, and there was no significant difference between severe IUAs tissue and normal myometrium (p&#x2009;>&#x2009;0.05). Transcriptomic and proteomic data revealed that genes and proteins involved in cell mitosis, such as KIF14, KIF4A, and CIT, were downregulated in both IUAs lesion tissues compared with the inner myometrium (p&#x2009;<&#x2009;0.05). Additionally, some genes or proteins that participate in activating the complement-coagulation cascade system and extracellular matrix (ECM) degradation also significantly differed (p&#x2009;<&#x2009;0.05). CONCLUSIONS: Transcriptomic and proteomic data revealed a correlation between endometrial injury and the myometrium. These findings preliminarily revealed that the myometrium possibly contributes to the aetiology and progression of IUAs through dual mechanisms. On the one hand, the myometrium inhibits endometrial regeneration by suppressing the cell mitogenic pathway. On the other hand, it promotes fibrosis by activating the complement-coagulation cascade system and inhibiting the ECM degradation pathway. These new findings increase our understanding of the pathogenesis of IUAs and potentially contribute to the application of precision clinical treatment for IUAs.

Humans↗