Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Production of a member of transforming growth factor-beta (TGF-beta) superfamily, activin A, was examined in the bone tissue by using reverse transcriptase polymerase reaction. As a result, specific bands were detected showing the presence of activin A mRNA in the bone tissues. In order to localize the production site of activin A in the bone tissues, we tried to immunolocalize activin A in fetal mouse calvaria cultured in a medium containing fetal calf serum, 1 alpha-25(OH)2 vitamin D2 and parathyroid hormone. In these cultured calvaria, bone tissues including bone-resorbing osteoclasts in vitro were observed. Positive staining demonstrating the presence of activin A resided inside of the multinucleated cells in the bone resorbing lacunae, suggesting the production of activin A in osteoclasts. Activin A was also localized immunohistochemically in the osteoclast-like multinucleated cells developed in vitro. These results suggest that osteoclast produce activin in the bone tissues and that activin may play some roles by autocrine and/or paracrine manner in bone metabolisms.
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PMID:Immunohistochemical detection of activin A in osteoclasts. 896 19

The aim of the present study was to evaluate whether spontaneous labor at term and pathological preterm labor are associated with changes in the expression of activin A and activin receptor mRNAs in fetal membranes. In addition, amniotic fluid activin A concentration in women delivering at term or undergoing preterm labor was also measured. The expression of activin beta A subunit and activin receptor type II and type IIB mRNAs was assessed by reverse transcriptase-PCR on specimens of amnion and chorion collected from patients delivering at term or undergoing preterm labor. Control specimens were collected from women delivered by elective cesarean section who had not experienced labor. A specific two-site ELISA was used to measure activin A concentrations in the amniotic fluid. A cross-sectional study of amniotic fluid retrieved by amniocentesis from 109 pregnant women was carried out. Patients were classified into the following groups: (1) healthy controls at term but not in labor (n = 25); (2) healthy controls at term in spontaneous labor (n = 40); (3) healthy controls between 23 and 36 weeks of gestation (n = 12); (4) patients in preterm labor responding to tocolytic treatment (n = 19); (5) patients in preterm labor with subsequent delivery (n = 13). Activin beta A subunit and activin receptor type IIB mRNA levels in both the chorion and amnion in women delivering at term or after preterm labor were significantly higher than in women delivering without undergoing labor (P < 0.01). Expression of activin receptor type II mRNA in membranes did not differ among the three groups of women. Amniotic fluid activin A concentration in patients in labor was significantly higher than in those at term but not in labor (P < 0.01). Patients in preterm labor had significantly higher amniotic fluid activin A concentrations than women at the same stage of gestation (P < 0.01). The highest values were found in women undergoing preterm labor and subsequent delivery. In conclusion, spontaneous labor and preterm labor are characterized by increased synthesis and release of activin A from amniotic and chorionic cells and by an augmented expression of activin type IIB receptor.
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PMID:High levels of fetal membrane activin beta A and activin receptor IIB mRNAs and augmented concentration of amniotic fluid activin A in women in term or preterm labor. 924 42

Ovarian surface epithelium (OSE) is the tissue of origin for the majority of ovarian cancers. The mechanism underlying the neoplastic transformation of OSE to ovarian cancer is poorly understood. Activin, a member of the transforming growth factor-beta superfamily, has been shown to increase cell proliferation in ovarian cancer cells. The present study was carried out to investigate the expression and regulation of activin/inhibin subunits and activin receptors in normal and neoplastic OSE. Using reverse transcriptase-polymerase chain reaction and Southern blot analysis, the mRNA levels of alpha, betaA and betaB subunits and activin receptor type IIA and IIB were analyzed in normal OSE and the ovarian cancer cell line, OVCAR-3 cells. The alpha and betaA subunits were highly expressed in normal OSE when compared to OVCAR-3 cells. By contrast, betaB subunit was highly expressed in OVCAR-3 cells, when compared to normal OSE cells. Interestingly, activin receptor IIB mRNA levels were significantly higher in OVCAR-3 when compared to normal OSE cells, whereas activin receptor IIA mRNA levels were the same in both cell types. To characterize the growth modulatory role of activin during neoplastic progression, normal OSE and OVCAR-3 cells were treated with recombinant human activin A (rh-activin A). At concentrations of 1,10 and 100 ng/ml, rh-activin A stimulated the growth of OVCAR-3 cells, but not of normal OSE. Treatment with follistatin, binding protein of activin, attenuates the stimulatory effect of activin. To determine whether the growth stimulatory action of activin in the neoplastic OSE is mediated via an autocrine regulatory mechanism, OVCAR-3 cells were treated with rh-activin A in a dose- and time-dependent manner and the expression levels of activin/inhibin subunits and activin receptors were investigated. Treatments with activin increased the alpha and betaA subunit mRNA levels in a dose- and time-dependent manner. However, no difference was observed in levels of betaB subunit, or in activin receptor type IIA and IIB mRNAs following activin treatments in OVCAR-3 cells. Taken together, these results suggest that different levels of activin/inhibin and activin receptor isoforms are expressed in normal and neoplastic OSE cells. In addition, the altered expression of the activin/inhibin subunits, as well as the cell proliferative effect of activin observed in OVCAR-3 but not in normal OSE cells, indicate that activin may act as an autocrine regulator of neoplastic OSE progression.
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PMID:Differential expression of activin/inhibin subunit and activin receptor mRNAs in normal and neoplastic ovarian surface epithelium (OSE). 1130 76

Peroxisome proliferators stimulate hepatocyte growth in rat liver in vivo. Activin A, a homodimer of inhibin betaA, inhibits DNA synthesis in hepatocytes. The inhibitory action of activin A is suppressed by follistatin, an activin-binding protein. In this paper, we investigated whether administration of di-n-butyl phthalate (DBP), a peroxisome proliferator, modifies the production of activin A and follistatin in rat liver by hourly monitoring of inhibin betaA and follistatin mRNA levels by reverse transcriptase polymerase chain reaction analysis. The mRNA levels of the other inhibin beta chains (inhibin betaB and betaC) were examined in a similar manner. The inhibin betaA mRNA level decreased to about 30% by 3 h after DBP administration (8.6 mmol/kg body weight), remained low until 12 h, and returned to its original level by 24 h. The follistatin mRNA level increased to about 2 times by 6 h, and returned to its original level by 24 h. The inhibin betaB mRNA had started to increase by 1 h, peaked at 6 h at about 4 times its initial level, and returned to its original level by 12 h. The inhibin betaC mRNA level had doubled by 6 h and it returned to its original level. These results indicate that the growth stimulatory action of peroxisome proliferators may be mediated via the decrease in activin A level and activity and suggest that the increases in follistatin as well as inhibin betaB and betaC chains may play a role in peroxisome proliferator-stimulated hepatocyte growth.
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PMID:Regulation of inhibin beta chains and follistatin mRNA levels during rat hepatocyte growth induced by the peroxisome proliferator di-n-butyl phthalate. 1223 Jan 21

Activin A (beta A beta A) and inhibin A (alpha beta A) are dimeric glycoproteins secreted from early to term pregnancy in the maternal circulation. They circulate in higher amounts in women with gestational hypertension and/or pre-eclampsia, the most important gestational diseases also causing fetal growth restriction (FGR). Since no data are available in patients with pre-eclampsia and superimposed FGR, by using two-site immunoassays we evaluated serum activin A and inhibin A levels in serum samples collected from: healthy normotensive pregnant controls (n = 42); and women with pre-eclampsia with (n = 19) or without superimposed FGR (n = 21). In addition, by quantitative reverse transcriptase-polymerase chain reaction the changes of alpha- and beta A-subunit mRNA expression in placentas collected from healthy controls (n = 7) and pre-eclamptic pregnancies with (n = 6) or without (n = 6) superimposed FGR was also investigated. Activin A and inhibin A serum levels were significantly higher in pre-eclampsia, and the presence of FGR did not significantly modify these concentrations. Similarly, inhibin-subunit mRNA levels in placentas from pre-eclampsia were significantly higher than in controls, and FGR did not significantly affect this expression. The present data suggest that the increased placental expression of inhibin subunit mRNAs is part of the mechanism leading to increased serum activin A and inhibin A levels.
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PMID:Pre-eclampsia with fetal growth restriction: placental and serum activin A and inhibin A levels. 1258 30

We have previously demonstrated that activin A at low concentrations induced ventral mesoderm including blood-like cells from Xenopus animal caps and that beating heart could be also induced from animal caps treated with 100 ng/ml activin A, suggesting that activin A might be involved in cardiac vasculogenesis. A vascular endothelial growth factor (VEGF) is a powerful mitogen for endothelial cells and is an inducer and regulator of angiogenesis. However, VEGF function in Xenopus development is not clearly identified. In this study, we determined the effect of VEGF on activin A-induced differentiation of animal cap. The VEGF induced duct-like structure composed of Flk-1-positive cells together with the induction of nonvascular tissues, such as neural tissues. This histological result was coincident with our reverse transcriptase-polymerase chain reaction analysis that VEGF together with activin A promoted the expression of Xenopus N-CAM and Xenopus brachyury. This study suggests that VEGF has additional biological activities besides angiogenesis, and arises a different function that VEGF induces stroma cell migration or recruitment that are required for blood vessel formation. This differentiation system will aid in the understanding of angiogenesis during early development.
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PMID:Modulation of activin A-induced differentiation in vitro by vascular endothelial growth factor in Xenopus presumptive ectodermal cells. 1602 71

Activins are members of the transforming growth factor-beta superfamily that exert neurotrophic and neuroprotective effects on various neuronal populations. To determine the possible function of activin in stroke injury, we assessed which components of the activin signalling pathway were modulated in response to middle cerebral artery occlusion (MCAO). Furthermore, because oestradiol replacement protects against MCAO-induced cell death, we explored whether oestradiol replacement influences activin gene expression. Female Sprague-Dawley rats underwent permanent MCAO and the expression of activins and their corresponding receptors was determined by semiquantitative reverse transcriptase-polymerase chain reaction at 24 h after onset of ischaemia. We observed up-regulation of activin betaA and activin type I receptor A mRNA in response to injury. Dual-label immunocytochemistry followed by confocal z-stack analysis showed that the activin A expressing cells comprised neurones. Next, we monitored the time course of activin betaA mRNA expression in oestradiol- or vehicle-treated rats at 4, 8, 16 and 24 h after MCAO via in situ hybridisation. Starting at 4 h after injury, activin betaA mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin betaA mRNA levels in the cortex increased dramatically with time and were highest at 24 h after the insult, and oestradiol replacement did not influence this increase.
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PMID:Stroke injury in rats causes an increase in activin A gene expression which is unaffected by oestradiol treatment. 1642 Feb 78

Steroid hormones, cytokines, and growth factors have a major role in evoking local endometrial changes needed for trophoblast implantation. In the present study, the effect of interleukin-1beta (IL-1beta), 17-beta estradiol (E2), and progesterone (Pr) on activin A and follistatin (FS) secretion from cultured human endometrial stromal cells (HESCs) is evaluated. HESCs were obtained from healthy human endometrial samples (n = 8) collected from healthy women. The cells were cultured and stimulated with E2 (10(-7) M, 10(-6)M), Pr (10(-7)M, 10(-6)M), IL-1beta (500 pg/mL), IL-1beta (500 pg/mL) + E2 (10(-6)M), and IL-1beta (500 pg/mL) + Pr (10(-6)M). Activin A and FS secretion and mRNA expression were assayed by enzyme-linked immunosorbent assay and semiquantitative reverse transcriptase-polymerase chain reaction, respectively. Pr (10(-7) M, 10(-6) M) significantly increased activin A secretion and mRNA expression from HESCs, but E2 did not show remarkable effects. The addition of IL-1beta (P< .001), IL- 1beta + E2 (P < .01), and IL-1beta + Pr (P< .001). significantly stimulated activin A secretion and mRNA expression, compared to untreated cells. Activin A expression and secretion after the coincubation of IL-1beta+ Pr were significantly higher than after IL-1betaand IL-1beta+ E2 stimuli ( P< .01 and P< .001, respectively). Neither Pr nor E2 and IL-1beta had a significant effect on FS secretion and expression. IL-1betaand Pr stimulated activin A but not FS secretion from cultured HESCs, and the effect of IL-1betawas augmented by Pr. These findings, together with the evidence that activin A is involved in trophoblast implantation, suggest the existence of a complex cross-talk by which the ovary, through Pr secretion, and the embryo, through IL-1beta production, may trigger the endometrial induction of activin A and consequently timing implantation.
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PMID:Interleukin 1beta and progesterone stimulate activin a expression and secretion from cultured human endometrial stromal cells. 1763 13

We investigated the toxic effects of carbendazim and n-butyl isocyanate (BIC), metabolites of the fungicide benomyl, on development in the African clawed frog, Xenopus laevis. To test the toxic effects, frog embryo teratogenesis assays using Xenopus were performed. Embryos were exposed to various concentrations of carbendazim (0-7 microM) and BIC (0-0.2 microM). LC(100) for carbendazim and BIC were 7 and 0.2 microM, respectively, and the corresponding LC(50), determined by probit analysis, were 5.606 and 0.135 microM. Exposure to carbendazim concentrations > or = 3 microM and BIC concentrations > or = 0.1 microM resulted in 10 different types of severe external malformation. Histological examinations revealed dysplasia of the brain, eyes, intestine, and somatic muscle, and swelling of the pronephric ducts. These phenomena were common in both test groups. The tissue-specific toxic effects were investigated with an animal cap assay. Neural tissues are normally induced at a high frequency by activin A, however, the induction of neural tissues was strongly inhibited by the addition of carbendazim. Conversely, the addition of BIC resulted in weak inhibition of neural tissues. Electron micrographs of animal cap explants revealed degeneration of cell junctions in the carbendazim-treated group, but not in the BIC-treated group. Numerous residual yolk platelets and mitochondrial degeneration were commonly observed in both test groups. The gene expression of cultivated animal cap explants was investigated by reverse transcriptase-polymerase chain reaction and revealed that expression of the neural-specific marker neural cell adhesion molecule was more strongly inhibited in the carbendazim-treated group than in the BIC-treated group.
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PMID:Toxic effects of carbendazim and n-butyl isocyanate, metabolites of the fungicide benomyl, on early development in the African clawed frog, Xenopus laevis. 1821 21

The SLIT/Roundabout (ROBO) pathway is involved in follicle development of mammalian ovary, and 2 secreted hormones activin A and inhibin A have potential roles in modulation of the SLIT/ROBO system, but the related actions remain poorly understood in bird. The aims of the present study were to examine the spatial and temporal expression of the SLIT ligand genes (SLIT1, SLIT2, and SLIT3) and their receptor ROBO1, ROBO2, ROBO3, and ROBO4 genes in various-sized prehierarchical follicles during hen ovary development and the effects of activin A and inhibin A on the expression of these genes in the cultured hen follicles. Our result demonstrated that the transcripts of the 3 SLIT genes were highly expressed in the developing follicles and expression patterns of the SLIT transcripts were different from those of ROBO genes detected by real-time quantitative reverse transcriptase PCR. Both SLIT and ROBO transcripts were predominantly expressed in oocytes and granulosa cells from the prehierarchichal follicles examined by in situ hybridization. The localization for SLIT and ROBO proteins was revealed by immunohistochemistry similar to the spatial distribution of their transcript. In cultured follicles (4 to 8 mm in diameter), the expression levels of SLIT and ROBO members are hormonally regulated by activin A (10 ng/mL) and/or inhibin A (20 ng/mL) after treatment for 24 h. However, the expression of only SLIT2, SLIT3, and ROBO3 mRNA presented a directly opposite response to activin A and inhibin A hormones. These results indicate that SLIT/ROBO pathway is implicated in the prehierarchical follicular development of the hen ovary by an intrafollicular autocrine and/or paracrine action, and is influenced by activin A and inhibin A hormones.
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PMID:New insights into implication of the SLIT/ROBO pathway in the prehierarchical follicle development of hen ovary. 2618 27


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