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)

Endothelin-1, a potent vasoconstrictor of cerebral vessels, is produced by rat primary astrocytes and is subject to autostimulatory regulation in these cells. In this study we examined the effect of thrombin on astrocytic endothelins and report that endothelin-1 is released into the culture fluid in response to thrombin treatment. However, increased production of endothelin-1 is not accompanied by a concomitant increase in steady-state levels of endothelin-1 mRNA as assessed by reverse transcriptase-polymerase chain reaction, even though thrombin stimulation leads to increased inositolphospholipid turnover and activation of the nuclear factor AP1. Thus, astrocytic production of endothelin-1 may be mainly post-transcriptionally regulated in response to thrombin stimulation. In addition, two endothelin receptor genes (ET(A) and ETB) were found to be transcribed simultaneously in primary astrocyte cultures, and both thrombin and endothelin-1 stimulation result in a distinct temporary decrease in ET(A) mRNA. These studies suggest a role for thrombin in the regulation of brain perfusion through astrocytic endothelin-1 expression.
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PMID:Thrombin is a regulator of astrocytic endothelin-1. 767 2

Endothelin 3 (EDN 3) and the endothelin receptor B (EDNRB) are involved in the development of neural crest and particularly of the melanocytes and the enteric nervous system. We reported previously that the avian EDNRB gene is expressed in the neural fold before crest cell migration and later on in all the neural crest derivatives except, at any developmental stage, in the melanocytic lineage. However, quail melanoblasts proliferate in response to EDN 3 stimulation in vitro. These observations prompted us to search for another type of endothelin receptor (EDNR). We report here the cloning by reverse transcriptase-PCR of an avian cDNA encoding a subtype of EDNR, which we have called EDNRB2, because its deduced amino acid sequence is more closely related to that of EDNRB than to either the mammalian EDNRA or to the Xenopus EDNRC. Its expression pattern differs from that of the "classical" avian EDNRB because it is strongly expressed in melanoblasts and melanocytes. EDNRB2 transcripts are also abundant in the liver and kidney. Our pharmacological studies showed that EDNRB2 binds with similar affinity to EDN 1, EDN 2, and EDN 3, further confirming that this receptor belongs to the B type, although it displays a low affinity for sarafotoxin-c, a known EDNRB-selective agonist.
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PMID:Cloning and characterization of a novel endothelin receptor subtype in the avian class. 950 Dec 9

The aim of this investigation was to determine whether the endothelin receptor subtype of a megakaryoblastic cell line (MEG-01) changes during culture passages as cells undergo maturation and differentiation. On early-passage cells, binding of [125I]endothelin-1 was completely inhibited by 1 microM BQ 123 (cyclo-[D-tryptophanyl-D-aspartyl-prolyl-D-valyl-leucyl]), but not by sarafotoxin 6C. Also the endothelin-1-enhancing effect on [Ca2+]i was prevented by BQ 123, whereas sarafotoxin 6C had no effect on [Ca2+]i. In late-passage cells, endothelin ET(B) analogs, unlike endothelin ET(A) analogs, competed with binding of [125I]endothelin-1. Endothelin ET(B) receptor agonists increased [Ca2+]i while the endothelin-1-induced response was inhibited by BQ 788 ([N-[(2R,6S)-2,6-dimethyl-piperidinocarbonyl]-4-methyl-D-leucyl]-[ N(omega)-(methoxycarbonyl)-D-tryptophanyl]-D-norleucine), but not by BQ 123, although both endothelin ET(A) and ET(B) receptor mRNAs were expressed, as shown by reverse transcriptase-polymerase chain reaction. These results demonstrate that in MEG-01 cells switch from expression of endothelin ET(A) to expression of ET(B) receptors during culture. The data also suggest that late-passage MEG-01 cells look like platelets, in terms of endothelin receptor subtype.
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PMID:Change of endothelin receptor subtype in the MEG-01 human megakaryoblastic cell line. 960 Jun 67

The biochemical and molecular endothelin-1 (ET-1) responses to high dose morphine sulfate infusion were studied in conscious newborn piglets (n = 6) that received a loading dose of 100 micrograms/kg over 5 min followed by a continuous i.v. infusion dose of 100 micrograms.kg-1.h-1 for 4 h. The control group (n = 6) received equivalent volume loading and infusion doses of 5% dextrose. Blood samples were drawn serially from the femoral artery and sagittal sinus vein before (0), during (30 min, 1, 2, 3, and 4 h), and post (1 and 2 h) infusion. Five micrograms of total RNA obtained from brainstem tissue homogenates was analyzed by reverse transcriptase--polymerase chain reaction (RT-PCR). The amounts of mRNA encoding ET-1, and endothelin receptor subtypes ETA and ETB, were semiquantitated using densitometric scanning. Morphine infusion resulted in elevated respiratory rate and mean arterial blood pressure, with no effect on arterial pH, Po2, and O2 saturation. Compared with the control group, morphine induced significant elevations in plasma ET-1 levels following the bolus dose (systemic: 13.2 +/- 3.6 vs. 8.6 +/- 2.2 pg/mL, p < 0.05; sagittal sinus vein: 13.7 +/- 3.4 vs. 8.2 +/- 0.9 pg/mL, p < 0.01). These effects lasted up to 2 h after discontinuation of morphine infusion (systemic: 14.5 +/- 3.4 to 18.7 +/- 5.7 pg/mL vs. 7.5 +/- 0.8 to 9.4 +/- 3.2 pg/mL, p < 0.05 to p < 0.01; sagittal sinus vein: 14.8 +/- 2.7 to 17.6 +/- 2.8 pg/mL vs. 7.5 +/- 1.4 to 9.4 +/- 3.4 pg/mL, p < 0.05 to p < 0.01). The RT-PCR assay showed a twofold (p < 0.02) upregulation in ET-1 and a threefold (p < 0.007) upregulation in ETA receptor mRNA expression in the brainstem of morphine-treated animals. In contrast, there was a threefold (p < 0.0001) downregulation of the ETB receptor mRNA expression. The rapid and sustained elevations in systemic arterial and sagittal sinus venous ET-1 levels suggest a role for ET-1 in the morphine-induced excitatory responses observed in newborn piglets. Upregulation of ETA receptors and downregulation of ETB receptors in the brainstem with high doses of morphine may indicate possible effects on cerebral vascular tone.
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PMID:Biochemical and molecular endothelin responses to morphine sulfate infusion in conscious newborn piglets. 979 54

In this study, reverse transcriptase polymerase chain reaction was used to amplify human endothelin receptor A (ETA) and ETB receptor mRNA. A truncated ETA receptor transcript with exons 3 and 4 skipped was found. The skipping of these two exons results in 109 amino acids being deleted from the receptor. The truncated receptor was expressed in all tissues and cells examined, but the level of expression varied. In melanoma cell lines and melanoma tissues, the truncated receptor gene was the major species, whereas the wild-type ETA was predominant in other tissues. A 1.9-kb ETA transcript was identified in melanoma cell lines by Northern blot, which was much smaller than the transcript in heart and in other tissues reported previously (4.3 kb). The cDNA coding regions of the truncated and wild-type ETA receptors were stably transfected into Chinese hamster ovary (CHO) cells. The truncated ETA receptor-transfected CHO cells did not show binding affinity to endothelin 1 (ET-1) or endothelin 3 (ET-3). The function and biological significance of this truncated ETA receptor is not clear, but it may have regulatory roles for cell responses to ETs.
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PMID:Truncated human endothelin receptor A produced by alternative splicing and its expression in melanoma. 982 Jan 69

Normal human melanocytes have been shown to respond to the signal peptide endothelin by increased proliferation and melanin formation. Contradictory findings, however, have been reported about which of the two endothelin receptors (EDNRA or EDNRB) is expressed in normal melanocytes and melanoma cells. Moreover it was not clear whether malignant cells differ from their normal precursors in this respect. Screening a melanocyte cDNA library for genes downregulated in melanomas identified clones specific for EDNRB. Northern blots proved that the corresponding mRNA is generally expressed in cultures of human cutaneous melanocytes and congenital melanocytic nevus cells. In 16 of 17 melanoma cell lines, however, the expression of EDNRB mRNA was strongly downregulated. EDNRA was only weakly expressed and detectable by northern blotting in 12 of 17 cultures of benign melanocytic cells and four of 17 melanoma cell lines. Nested reverse transcriptase-polymerase chain reaction proved several melanoma cell lines to be completely negative for EDNRA expression. Gene deletion as the cause of missing endothelin receptor expression was ruled out by genomic Southern blots. Receptor binding assays confirmed RNA data revealing 1.6 x 105 endothelin-1 binding sites per cell for a melanocyte culture and between 8.7 x 104 and 400 sites per cell for melanoma cell lines. Expression of pigmentation genes coding for tyrosinase, TRP-1 and TRP-2 correlated positively with that of EDNRB but negatively with EDNRA expression. EDNRB but not EDNRA expression is therefore typical for melanocytic cells, and downregulation of EDNRB seems to be an important characteristic of melanoma cells possibly related to malignancy or apoptosis.
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PMID:Downregulation of endothelin B receptor in human melanoma cell lines parallel to differentiation genes. 1038 40

Several studies have suggested an important role for the endothelin (ET) family of peptides in the vascular regulation of the nose. In addition, there is increasing evidence that ETs play a role in allergic airway inflammation. Endothelin is produced locally in the nose and mediates its effects via two distinct receptor subtypes, termed ET(A) and ET(B). Using reverse transcriptase-polymerase chain reaction, mRNAs encoding ET(A)- and ET(B)-receptors were detected in the human lower turbinate and sinus mucosa. The possibility of local release of ETs in connection with specific target receptors suggests a role for endothelin in the regulation of vascular tone, glandular secretion and epithelial functions.
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PMID:Expression of endothelin A- and B-receptors in human nasal mucosa. 1058 6

Meningiomas are common central nervous system neoplasms that exhibit remarkably diverse histopathology and biological behavior. Compared to astrocytomas, the most common central nervous system tumor, little is known about the molecular pathways critical for meningioma tumor formation and malignant progression. As an initial step toward characterizing the genetic basis of meningioma pathogenesis, we assessed cancer-related gene expression profiles of nonneoplastic leptomeningeal specimens and human meningiomas of varying World Health Organization (WHO) grade using high-density oligonucleotide microarrays. Although expression profile differences between nonneoplastic and meningioma specimens were readily discernible, the expression profile of a subset of genes could also distinguish WHO grade I from WHO grades II and III tumors. Altered expression levels of several genes identified in this study have been previously noted in meningiomas (eg, growth hormone receptor, IGFBP-7, endothelin receptor A, IGF2). However, we also identified a number of novel genes whose expression was associated with WHO grade and was confirmed by reverse transcriptase-polymerase chain reaction in a larger, independent set of meningeal tumors (n = 47). This report represents the first gene expression profiling studies of meningiomas and identifies some initial candidate genes that may provide further insights into the genetic basis for meningioma pathogenesis.
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PMID:Molecular characterization of human meningiomas by gene expression profiling using high-density oligonucleotide microarrays. 1216 91

Tumours of the Ewing's sarcoma (ES) family and neuroblastoma (NBL) were examined by reverse transcriptase-PCR for expression of mRNA for endothelin (ET) receptors ET-A and ET-B, and the ligands ET-1, ET-2 and ET-3. The effect of ET-1, ET-3, an ET-1-neutralizing antibody and ET-A receptor antagonist BQ-123 on cell proliferation was examined using an ELISA. Loss of ET-B receptor mRNA occurred in 57% of ES and 42% of NBL tumours. This appeared to be associated with the presence of metastatic disease and disease progression. ET-A receptor mRNA was expressed in all ES and 85% of NBL tumours, and in all ES and NBL cell lines examined. All ET ligands were detected in NBL cell lines, but only ET-1 and ET-2 were expressed in ES cell lines. Treatment of ES and NBL cells with ET-1 increased proliferation, but ET-3 had no effect. Incubation of ES and NBL cells with an ET-1-neutralizing antibody or BQ-123 decreased proliferation. The ET-3 ligand and ET-B receptor may be associated with migration and metastasis of ES and NBL, whereas ET-1 (acting through the ET-A receptor) may regulate their proliferation.
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PMID:Endothelins may modulate invasion and proliferation of Ewing's sarcoma and neuroblastoma. 1219 14

Since both endothelin-1 (ET-1) and aldosterone have been shown to induce expression of several pro-inflammatory genes, including cyclooxygenase-2 (COX-2), in the vasculature as a cardiovascular risk hormone, the present study was undertaken to examine the effects of ET-1 and aldosterone on COX-2 gene expression as measured by a real-time reverse transcriptase-polymerase chain reaction in aortic endothelial cells. Treatment with ET-1(10 M) markedly upregulated COX-2 mRNA levels in rat endothelial cells, whereas aldosterone (10 M) did not show any effect. The ET-1-induced COX-2 upregulation was inhibited by pretreatment with a non-selective endothelin receptor antagonist (TAK044), a protein kinase C inhibitor (GF109203X), and a MEK inhibitor (PD98059). Furthermore, ET-1 increased intracellular reactive oxygen species generation as estimated by the measurement of dichlorofluorescein fluorescence, whose effect was blocked by a COX-2 inhibitor (NS398). Our data show that ET-1 induces COX-2 upregulation in rat endothelial cells via a protein kinase C-dependent and extracellular signal-regulated kinase-dependent pathway, which may largely contribute to the generation of intracellular reactive oxygen species.
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PMID:Endothelin-1 induces cyclooxygenase-2 expression and generation of reactive oxygen species in endothelial cells. 1583 13


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