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)

We studied the involvement of annexin V in the antiproliferative effects of gonadotropin-releasing hormone (GnRH) agonists on human endometrial cancer cell line HHUA. HHUA cell line expressed mRNA for GnRH receptors as assessed by reverse transcriptase-PCR with oligonucleotide primers. In the presence of buserelin, the proliferation of this cell line was significantly (P < 0.01) reduced to 60% of control after 72 hr. Peak intracellular concentrations of annexin V, equivalent to about twice the control value, were obtained after 48 hr exposure to buserelin. Intracellular annexin V concentration was increased not only by buserelin, but also by protein kinase C (PKC) activator. However, there was no increase in intracellular annexin V concentration when cells were incubated with PKC inhibitor before the addition of buserelin. The results suggest that GnRH agonists inhibit cell proliferation by increasing intracellular concentrations of annexin V, an effect mediated by the activation of PKC.
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PMID:Involvement of annexin V in antiproliferative effects of gonadotropin-releasing hormone agonists on human endometrial cancer cell line. 926 65

The binding of gonadotropin-releasing hormone (GnRH) to its receptor in the anterior pituitary gland is the key molecular interaction regulating the reproductive process of mammals. Here, we report the isolation of a cDNA representing this receptor from rat anterior pituitary and the regulation of expression of its mRNA. The rat GnRH receptor cDNA was composed of 2909 nucleotides and encoded a protein containing 327 amino acids having a seven transmembrane topology. Northern blot analysis on RNA from rat pituitary, ovary and testis showed four different transcripts (5.0, 4.5, 2.5 and 1.3 kb) of which the 5.0 kb form was most abundant. The levels of expression of the transcripts were found to be highest in the pituitary followed by the ovary and the testis (about 40% and 5% compared to pituitary, respectively). Using the more sensitive reverse transcriptase/PCR technique, we also detected GnRH receptor mRNA in the adrenal and the hypothalamus. Measurement of pituitary GnRH receptor mRNA levels (the 5.0 kb form) during the estrous cycle showed the lowest levels at estrus (1.0-fold), a 2.2 +/- 0.57 (mean +/- SEM) -fold increase at diestrus I, a 3.5 +/- 0.41-fold increase at diestrus II, a 2.6 +/- 0.34-fold increase on the morning of proestrus, and a 1.9 +/- 0.25-fold on the afternoon of proestrus. Removal of the ovaries led to a 2.7 +/- 0.29-fold increase in GnRH receptor mRNA levels in the pituitary gland; treatment of ovariectomized rats with estrogen resulted in a significant decrease in GnRH receptor mRNA levels. Our studies demonstrate ovarian regulation of GnRH receptor mRNA expression in the anterior pituitary gland.
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PMID:Rat gonadotropin-releasing hormone (GnRH) receptor: tissue expression and hormonal regulation of its mRNA. 939 47

The androgen dependency of the genes coding for the cysteine-rich secretory proteins (CRISP) was analysed in their main sites of expression. Male mice were treated with the gonadotropin-releasing hormone antagonist Ac-DNapAla-DClPhAla-DPyrAla-Ser-Tyr-DCtl-Leu-Lys (Mor)-Pro-DAla-NH2 [DNapAla, D-2-naphthyl-Ala; DClPhAla, D-4-chlorphenyl-Ala; DPyrAla, D-pyridyn-3-yl-Ala; DCtl, D-citrulline; Lys(Mor), L-2-amino-6-(morpholin-4-yl)-hexanoic acid], and CRISP RNA levels were assessed by northern blot and competitive reverse transcriptase-mediated (RT)-PCR. In the salivary gland, CRISP-1 and to a lesser extent CRISP-3 expression was markedly reduced, in spite of an up-regulation of androgen receptor transcript levels. A down-regulation of CRISP-1 expression was also observed in the epididymis. Conversely, the levels of the testicular CRISP-2 transcripts were hardly affected at all. Female mice were ovariectomised and treated with testosterone propionate, and their salivary gland RNAs analysed. CRISP-1 and CRISP-3 RNA levels were significantly increased, and these effects were prevented by a concomitant treatment with the antiandrogen flutamide. Androgen receptor transcript levels were not affected by androgen administration but increased following antiandrogen treatment. CRISP expression during postnatal development was monitored by northern blot analysis. CRISP-1 and CRISP-2 transcripts were detected as early as 22 days after birth in the epididymis and testis, respectively, whereas CRISP-3 mRNA was visible only from day 30 in the salivary gland. A sharp increase of all CRISP levels was noted on day 40, coincident with the onset of sexual maturity. Altogether these results indicate that despite their high similarity, the CRISP genes are differentially regulated by androgens.
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PMID:Differential androgen regulation of the murine genes for cysteine-rich secretory proteins (CRISP). 942 96

Recent demonstrations of no changes in hypothalamic gonadotropin releasing hormone (GnRH) gene expression and GnRH levels detected at the pituitary gland in diestrous and lactating rats, indicate that lactational hypogonadotropism in this species is not associated with inhibition of hypothalamic GnRH synthesis and secretion. Hypothalamic galanin potentiates GnRH effects on luteinizing hormone (LH) secretion in male and cycling rats. To explore the interaction between GnRH and galanin during lactation, we studied in vitro the effects of pulsatile stimulation with those peptides upon LH synthesis and secretion from rat pituitaries on diestrous 1 or day 10 of lactation. Hemipituitaries were separately incubated in 1 ml Dulbecco's Minimal Essential Medium supplemented with 1% penicillin-streptomycin and fetal calf serum, at 37 degrees C in 5% CO2-air. The hemipituitaries were stimulated during 12 h with hourly pulses, 6 min each, of (a) gonadotropin releasing hormone (GnRH 25 ng/pulse), (b) rat galanin (600 ng/pulse), (c) GnRH plus galanin, or (d) saline. Medium was collected before each pulse to determine LH by radioimmunoassay. After the 12 h pulsatile regime total RNA was extracted and both actin and beta-LH mRNA were determined by reverse transcriptase polymerase chain reaction. There was a significant stimulation of LH secretion by GnRH (ANOVA, p < 0.001) without significant differences between diestrous and lactation pituitaries. Galanin alone did not modify LH secretion but it potentiated the effect of GnRH upon pituitaries from diestrous (p = 0.036) but not lactating rats. Neither peptide alone or its combination modified pituitary beta-LH mRNA levels. Results show that galanin regulates differently the secretion and synthesis of LH at the pituitary level. The disappearance of galanin-induced potentiation of GnRH effects upon LH secretion during lactation might contribute to the hypogonadotropism of lactation in the rat.
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PMID:Lactation inhibits the potentiating effect of galanin upon the GnRH-induced LH release observed in diestrous-1 rat. 1002 99

Six endometrial cancer cell lines (Ishikawa, EIIL, HEC1A, 6, 50 and 59), one breast cancer cell line (MCF-7) and two ovarian cancer cell lines (OVHS-1, HRA) were treated for 24 or 168 h with a gonadotropin-releasing hormone (GnRH) analogue, Buserelin acetate, and the cellular growth profile was studied. All these cell lines except for the HRA line had positive GnRH receptor mRNA expression detected by reverse transcriptase polymerase chain reaction. GnRHa suppressed cell growth after 168 h of exposure, but not after 24 h. Suppression of cell growth by the exposure to cis-platinum (CDDP, 10 nM for 24 h) was significantly increased in the presence of GnRHa for 168 h. The mechanism of this growth inhibition was tested by examining both RNA components of human telomerase (hTR) expression and telomerase activity. The results showed that GnRHa inhibits telomerase activity without altering the RNA component of telomerase expression. The present data suggest that GnRH analogue may modulate endometrial, breast and ovarian cancer cell growth through modifying the telomerase activity. Since GnRHa increased the cytotoxic effects of CDDP and GnRHa is a compound of high patient compliance, the value of GnRHa as a tumor sensitizer to CDDP should be further tested in clinical trials.
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PMID:In vitro effects of gonadotropin-releasing hormone (GnRH) analogue on cancer cell sensitivity to cis-platinum. 1038 Nov 37

Uterine leiomyomas develop from uterine smooth muscle cells, which are known to be regulated by estrogen and other growth factors. The purpose of this study was to investigate the role of expression of parathyroid hormone related-peptide (PTHrP) in the growth of uterine leiomyomas treated or untreated with gonadotropin-releasing hormone agonist (GnRH-a). Thirty-nine leiomyoma tissues were obtained from 36 patients who had been treated with GnRH-a (n=10) or without GnRH-a (n=29). The intensity of PTHrP immunostaining was categorized into three grades; "negative", "weakly positive", and "positive". Leiomyoma cell growth was estimated by the proliferating cell nuclear antigen (PCNA) labeling index (LI) with an image analyser. We also investigated the correlation between PTHrP expression and cell proliferation or histopathological findings. In the GnRH-a-untreated group, LI of the PTHrP "positive" group was significantly higher than that of the PTHrP "negative" group, but the intensity of PTHrP immunostaining did not correlate with LI in the GnRH-a-treated group. PTHrP expression did not correlate with histological findings or clinical parameters (age and phase of menstrual cycle) in either the GnRH-a-treated or the -untreated group. In addition, the expression of mRNA for PTHrP and its receptor was detected in leiomyomas by reverse transcriptase-polymerase chain reaction (RT-PCR). Our results indicate that the expression of PTHrP in leiomyomas correlated positively with cell growth in the GnRH-a-untreated group, suggesting that PTHrP may act as a local cell growth modifier in an autocrine/paracrine fashion on uterine leiomyomas.
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PMID:Involvement of parathyroid hormone-related peptide in cell proliferation activity of human uterine leiomyomas. 1042 71

The present study examined the effects of continuous treatment with gonadotropin-releasing hormone (GnRH) on GnRH receptor (GnRH-R) mRNA levels in dispersed cultures of rat pituitary cells. Pituitary GnRH-R mRNA levels were determined by competitive reverse transcriptase polymerase chain reaction. When pituitary cells were continuously exposed to a low dose of GnRH (0.2 nM), GnRH-R mRNA levels were transiently increased. The levels of GnRH-R mRNA were significantly increased up to 6 h and diminished to untreated levels by 24 h. Luteinizing hormone (LH) release was also increased significantly up to 12 h, maintaining similar levels in LH release thereafter. When GnRH antagonist ([D-pGlu1, D-Phe2, D-Trp3,6]-LH-RH) was added to the cultures together with GnRH (0.2 nM) for 6 h, the stimulatory effect of GnRH on GnRH-R mRNA levels and LH release was significantly diminished in a dose-related manner. In another experiment, pituitary cells were treated with various doses of GnRH (0.02-200 nM) for a relatively short (6 h) or a longer (24 h) period. When pituitary cells were exposed for 6 h, all doses of GnRH (0.02-200 nM) significantly increased GnRH-R mRNA levels in a dose-dependent manner. By contrast, continuous exposure to GnRH for 24 h was ineffective in changing pituitary GnRH-R mRNA levels at any given doses. These results indicate that the duration of GnRH treatment is critical for upregulation of GnRH-R mRNA by continuous GnRH. When pituitary cells were treated for 6 h with either a continuous mode of GnRH (0.2 nM) or an hourly pulsatile mode of GnRH (0.2 nM, 6 min/h), both treatments significantly augmented GnRH-R mRNA levels. Thus, the modes of GnRH application, if treated for a relatively short period, do not appear to make a significant difference in upregulation of GnRH-R mRNA levels. Collectively, our data provide strong evidence that continuous GnRH application is able to upregulate pituitary GnRH-R mRNA levels, if treated for a relatively short period (6 h).
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PMID:Homologous upregulation of GnRH receptor mRNA by continuous GnRH in cultured rat pituitary cells. 1066 41

Previous work has indicated that, during the process of gametogenesis in salmon, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are differentially synthesized and released. Although substantial information is available on the regulation of LH in many fish species, relatively little is known about the regulation of FSH biosynthesis and secretion or the regulation of two types of alpha subunit in salmon. In this study, the effects of salmon gonadotropin-releasing hormone (sGnRH) on in vitro secretion of FSH, and alpha1, alpha2, LH beta, and FSH beta subunit gene expression were investigated in coho salmon (Oncorhynchus kisutch) using primary pituitary cell cultures. To quantify FSH beta, LH beta, alpha1, and alpha2 subunit transcript levels, a multiplex RNase protection assay (RPA) was developed. Probes for the beta subunits of coho salmon FSH and LH were available from previous studies. To generate probes for the alpha subunit RPAs, alpha1 and alpha2 subunit cDNAs were cloned using reverse transcriptase PCR. Release of FSH and LH into cell culture medium was quantified by radioimmunoassays. The effects of sGnRH on gonadotropin release and gene expression were tested at two points during the spring (April and May) prior to spawning in the autumn; a period when plasma and pituitary FSH levels are increasing and females are in early stages of secondary oocyte growth. In both experiments, sGnRH increased steady-state mRNA levels of FSH beta, alpha1, and alpha2, whereas LH beta mRNA levels were not detectable. Secretion of FSH was stimulated by sGnRH in a concentration-dependent manner. Medium LH was not detectable in the first experiment (April) and was measurable only after sGnRH treatment in the second experiment (May). Control levels of medium FSH and transcripts for FSH beta and alpha1 subunits increased approximately fourfold between April and May, whereas alpha2 transcript levels remained relatively constant, suggesting that the seasonal increase in FSH release may involve increased production of alpha1. Therefore, sGnRH has direct stimulatory effects on both secretion of FSH and FSH subunit biosynthesis, most likely due to increased transcription. However, alterations in rates of transcript degradation cannot be ruled out.
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PMID:Effects of salmon gonadotropin-releasing hormone on follicle stimulating hormone secretion and subunit gene expression in coho salmon (Oncorhynchus kisutch). 1084 95

We report the clinical evolution of a prostate cancer, metastasizing to lungs and bones, recurring locally, and escaping from anti-androgen therapy. Key event of biological progression of the patient's tumor was the coincidence of allelic imbalance accumulation and of bone metastases occurrence. The recurrent tumor was established as the transplantable xenograft PAC120 in nude mice, where it grew locally. PAC120 displayed the same immunophenotype of the original tumor (positive for keratin, vimentin, prostatic acid phosphatase, and Leu-7) and expressed human HOXB9, HOXA4, HER-2/neu, and prostate-specific antigen genes, as detected by reverse transcriptase-polymerase chain reaction. It formed lung micrometastases detected by mRNA expression of human genes. Cytogenetic analysis demonstrated numerous alterations reflecting the tumor evolution. PAC120 was still hormone-dependent; its growth was strongly inhibited by the new gonadotropin-releasing hormone antagonist FE 200486 but weakly by gonadotropin-releasing hormone superagonist D-Trp(6)-luteinizing-hormone releasing hormone (decapeptyl). Tumor growth inhibition induced by anti-hormone therapy was linked to the hormone deprivation degree, more important and more stable with FE 200486 than with D-Trp(6)-luteinizing-hormone releasing hormone. Surgical castration of mice led to tumor regressions but did not prevent late recurrences. Transition to hormone-independent tumors was frequently associated with a mucoid differentiation or with a neuroendocrine-like pattern. Independent variations of mRNA expression of HER-2/neu and prostate-specific antigen were observed in hormone-independent tumors whereas HOXB9 gene expression was constant. In conclusion, PAC120 xenograft, a new model of hormone-dependent prostate cancer retained the progression potential of the original tumor, opening the opportunity to study the hormone dependence escape mechanism.
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PMID:Clinical and experimental progression of a new model of human prostate cancer and therapeutic approach. 1148 33

The present investigation has examined which subunits of the GABA(A) receptor are expressed by gonadotropin-releasing hormone (GnRH) neurons in the juvenile and adult male mouse. Cells of defined morphology, located in the medial septum (MS) and rostral preoptic area (POA), were patch-clamped in the acute brain slice preparation and their cell contents extracted. A reverse transcriptase polymerase chain reaction (RT-PCR) procedure using nested primers was used to establish individual GnRH mRNA-expressing cells which were then evaluated for eleven GABA(A) receptor (alpha1-5, beta1-3, gamma1-3) subunit transcripts. Single and multiple GABA(A) receptor subunit mRNAs were detected in approximately 70% of all GnRH neurons. A range of different subunit mRNAs (alpha1, alpha2, alpha5, beta1, beta2, beta3, gamma2) were found in juvenile GnRH neurons, with the alpha1gamma2 and alpha5gamma2 combinations encountered most frequently within individual cells. The expression profile in adult GnRH neurons was more extensive than that detected in juveniles with alpha1, alpha2, alpha3, alpha5, beta1, beta2, beta3, gamma1 and gamma2 subunits all being detected. The major difference in subunit profile between GnRH neurons located in the MS and POA involved the beta subunits. The principal postnatal developmental change was one of increasing overall subunit heterogeneity in maturing POA GnRH neurons. The profile of GABA(A) receptor subunit mRNAs detected in male GnRH neurons was quite different to that reported by us for female GnRH neurons in the mouse using the same RT-PCR approach. Together, these findings indicate that postnatal GnRH neurons are likely to express a range of GABA(A) receptor subunit mRNAs in a sexually dimorphic and developmentally-regulated manner.
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PMID:Profiling gamma-aminobutyric acid (GABA(A)) receptor subunit mRNA expression in postnatal gonadotropin-releasing hormone (GnRH) neurons of the male mouse with single cell RT-PCR. 1169 62


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