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 addressed the role of soluble Fas (sFas), which suppresses Fas-mediated apoptosis, in the pathogenesis of Graves' disease (GD). The serum concentration of sFas was measured by enzyme-linked immunosorbent assay and the expression of sFas mRNA in thyroid tissues by reverse transcriptase-polymerase chain reaction. The serum concentration of sFas was significantly increased in untreated GD (mean+/-SD: 1.57+/-0.48 ng/mL) compared to age-matched control subjects (0.77+/-0.46 ng/mL). The serum sFas level tended to decrease after the medication of antithyroid drugs for 6 to 8 weeks and was significantly decreased in patients who were euthyroid for more than 3 years (0.98+/-0.23 ng/mL), compared to that in untreated GD. The concentration of serum sFas was significantly correlated with anti-thyrotropin (TSH) receptor antibody titers, but not with the other clinical parameters (free triiodothyronine [FT3], free thyroxine [FT4], TSH, antithyroglobulin antibody titer, antimicrosomal antibody titer, or 123I uptake). The sFas mRNA was detected in thyroid tissue, cultured thyrocytes, and intrathyroidal lymphocytes. sFas was detected in supernatant of cultured thyrocytes from patients with GD. Its production by thyrocytes was induced by culture with interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha). The present study confirms serum sFas increases in GD and provides evidence of local production of sFas by thyrocytes and its regulation by cytokines. These data suggest that sFas may play a role in the pathogenesis of GD.
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PMID:Increased serum soluble Fas in patients with Graves' disease. 1031 38

There is a controversy regarding whether there are thyrotropin (TSH) receptors in orbital fat and eye muscle tissues that may play a role in the pathogenesis of Graves' ophthalmopathy. To elucidate whether there are TSH receptors in orbital fat and eye muscle tissues in patients with Graves' ophthalmopathy, we applied the method of in situ hybridization in orbital fat and eye muscle tissues obtained during the operation for patients with Graves' ophthalmopathy, to directly detect TSH receptor mRNA. To identify whether the cells with positive TSH receptor mRNA are fibroblasts, we also did vimentin immunoreactivity study. To further prove the transcript does have a full length of TSH receptor, the samples of total RNA preparations, extracted from orbital fat and eye muscle tissues, were used as a template for reverse transcriptase polymerase chain reaction (RT-PCR) using three primer sets to generate cDNA fragments and cloned for sequencing. The results showed that the expression of TSH receptor mRNA was demonstrated in adipocytes and fibroblasts of orbital fat, and perimysial fibroblasts within eye muscle tissues by in situ hybridization and vimentin immunoreactivity study. Also, by using the RT-PCR, cloning and sequencing, we further proved that the transcript does have a full length of TSH receptor. The present study suggested that there are TSH receptors expressed in orbital fat and eye muscle tissues.
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PMID:Demonstration of thyrotropin receptor mRNA in orbital fat and eye muscle tissues from patients with Graves' ophthalmopathy by in situ hybridization. 1034 63

The influence of thyroid hormones on human adipose tissue leptin production and leptin gene expression was investigated in vitro and in vivo. Twelve women received 60 microg triiodothyronine (T3) per day for 7 days, which increased total T3 by 195% (1.78 +/- 0.07 to 5.25 +/- 0.39 mU/L, P < .001), significantly decreased thyrotropin ([TSH] 1.57 +/- 0.40 to 0.03 +/- 0.01 mU/L, P < .01), and increased energy expenditure (1,602 +/- 32 to 1,754 +/- 34 kcal/24 h, P < .05). However, serum leptin did not change (9.36 +/- 1.6 v 8.90 +/- 1.3 microg/L, nonsignificant). Human subcutaneous adipose tissue biopsies from eight healthy women were incubated in vitro as small fragments with T3 in concentrations from 1 to 50 nmol/L. Leptin production was inhibited dose-dependently. After 24 hours of incubation, a T3 concentration of 50 nmol/L reduced basal leptin production by 42% (P < .05) and the stimulated leptin production (dexamethasone 10 nmol/L) by 52% (P < .05). Leptin mRNA expression was measured by a semiquantitative multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) method. Fifty nanomolars T3 decreased basal leptin mRNA expression by 47% compared with controls (P < .001), and the stimulated leptin mRNA expression was reduced to a similar degree (53%). In conclusion, in human adipose tissue, T3 (>20 nmol/L) inhibited leptin production and leptin gene expression in vitro, whereas an elevation of T3 corresponding to a moderate thyrotoxic state (T3 5.25 +/- 0.39 nmol/L) was without any impact on serum leptin levels in vivo.
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PMID:Regulation of leptin by thyroid hormone in humans: studies in vivo and in vitro. 1059 95

Leptin receptor (leptin-R) is a polypeptide consisting of a single transmembrane-spanning component. Recent studies performed by reverse transcriptase polymerase chain reaction (RT-PCR) have shown the production of leptin-R in various tissues including the pituitary, hypothalamus and reproductive organs. The localization of leptin-R protein in the pituitary gland, however, has not been extensively studied. This study deals with the expression of leptin-R in the normal rat pituitary gland, which was disclosed primarily in the plasma membrane fraction by immunoblotting and immunohistochemical staining methods. Double immunohistochemical staining revealed that the colocalization of leptin-R and anterior pituitary hormone expression was seen mainly in growth hormone (GH)-secreting cells (97.4 +/- 1.3%; GH-positive cells/leptin-R-positive cells), but in less than 1% of prolactin (PRL)-, adrenocorticotropic hormone (ACTH)-, thyroid-stimulating hormone-beta (TSH beta)- and follicle-stimulating hormone-beta (FSH beta)/luteinizing hormone-beta (LH beta)-positive cells. In contrast, leptin was localized most frequently in FSH beta/LH beta- and less frequently in TSH beta-positive cells. The above findings suggest that, in the rat anterior pituitary gland, there are paracrine relationships between leptin-producing cells and cells with leptin-R, which may regulate the function of GH cells.
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PMID:Expression and localization of leptin receptor in the normal rat pituitary gland. 1157 88

We produced transgenic mice carrying a fusion gene (TTP-5) consisting of a 5.2-kbp segment of the 5' flanking sequence of the human thyrotropin beta-subunit (TSH beta) gene linked to the simian virus 40 large T antigen (SVT) gene. These mice developed pituitary tumors 6 months after birth and wasted away. With the 5.2-kbp TSH beta 5' flanking region governing SVT expression, SVT mRNA was present in the pituitary and testis but not in other tissues, as detected by the reverse transcriptase-polymerase chain reaction. Histological and immunohistochemical analyses showed that the pituitary tumors of the transgenic mice were composed of moderately differentiated pituitary cells that expressed TSH, growth hormone, and prolactin. These results indicate that the 5.2-kbp segment of the human TSH beta 5' regulatory region is sufficient to drive expression of SVT and induce tumorigenesis of hormone-producing pituitary cells in transgenic mice.
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PMID:Targeting oncogenesis by introduction of a 5.2-kbp segment of the 5' regulatory region of the human thyrotropin beta-subunit gene. 1179 63

Resistance to thyroid hormone (RTH) is a clinical syndrome characterized by elevated serum thyroid hormone (TH) levels, unsuppressed thyrotropin (TSH) levels, and tissue hyposensitivity to TH. In almost all cases, the genetic basis of RTH lies in mutation of one of the two TH receptor beta (TRbeta) alleles. Recently, patients from several families with phenotypic manifestations of RTH in the absence of TR mutations have been described. We report a case of a 31-year-old woman who presented with goiter, tachycardia, elevated TH levels, unsuppressed TSH, and "inappropriately normal" levels of peripheral TH action markers. In two separate clinical evaluations, the patient exhibited typical clinical and biochemical evidence for peripheral and pituitary RTH. Surprisingly, reverse transcriptase-polymerase chain reaction (RT-PCR) of full-length TRalpha and TRbeta mRNAs, and genomic PCR using primers flanking exons encoding the carboxy-terminal region of TRbeta failed to demonstrate mutations in the TRalpha or TRbeta genes. It is likely that defects in the regulation of TR genes or mutations in transcriptional cofactors involved in TR signaling account for this patient's phenotype.
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PMID:Resistance to thyroid hormone in a patient without thyroid hormone receptor mutations. 1183 36

Extra-thyroidal thyrotropin (TSH) receptors (TSHRs) have been demonstrated in several tissues and cells, including human and rat osteosarcoma cell lines. We have explored whether human TSHR (hTSHRs) also are present in primary cultures of human osteoblast-like (hOB) cells. [(125) I]TSH binding was limited in hOB cells, but somewhat higher in UMR 106-01 cells and considerably higher in hTSHR-transfected CHO cells. In hOB cells, the basal intracellular cAMP levels increased 282% after stimulation with 10 U/L TSH. In the hTSHR-transfected CHO cells, the cAMP increase was 3030% in response to 10 U/L TSH and 1240% after 1 U/L TSH. Free cytoplasmic calcium did not change in response to TSH in hOB cells. HTSHR mRNA was detected in hOB cells from 3/4 bone by reverse transcriptase polymerase chain reaction RT-PCR and nucleotide sequencing HTSHR mRNA, but could not be demonstrated with the RNase protection technique in hOB cells from 5 different donors. In conclusion, even after the use of several methods, we have found only weak evidence for expression and presence of functionally active hTSHR in hOB cells. Given the low level of expression, specific binding and cAMP signaling, we suggest that it is unlikely that circulating TSH plays a physiological role for bone metabolism mediated through osteoblasts.
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PMID:Weak evidence of thyrotropin receptors in primary cultures of human osteoblast-like cells. 1496 Dec 13

Usually thyroid cells isolated from tissue obtained by surgery or thyroid cell lines are used to investigate the pathogenesis of autoimmune thyroid diseases. Isolation and cultivation of thyrocytes from fine-needle aspiration biopsy (FNAB) has not yet been published. The aim of this study was to isolate and cultivate thyrocytes from samples of FNAB. FNAB samples were obtained from nine adults and nine children with Hashimoto's thyroiditis (HT). The aspiration material was filtered resulting in small samples of tissue on the surface of the filter membrane. These tissue fragments were digested by collagenase I and dispase II. The yielding cells were cultivated for 3 weeks in Ham's F12 Kaighn's Modification medium in presence of 1 mU/mL bovine thyrotropin (TSH), 10 microg/mL human insulin, 6 microg/mL transferrin, and 10(-8) M hydrocortisone. Finally, isolated thyroid cells were characterized by determination of gene expression of thyrotropin receptor (TSHR), thyroperoxidase (TPO), and thyroglobulin (Tg) using a nested reverse transcriptase-polymerase chain reaction (RT-PCR). Thyroid cells obtained by FNAB can be maintained over a time period of approximately 3 weeks. Depending on the sample size a final number of 1000-14,000 cells was gained per FNAB. In addition, all cells isolated by the described method expressed TPO mRNA. TSHR mRNA was found in 4 samples, whereas 15 samples were Tg mRNA-positive. There were no differences with respect to the expression TSHR and TPO mRNA between samples from adults and children. The isolation and cultivation of thyroid cells obtained by FNAB has been established. In contrast to surgical specimen, this technique provides an easy access to thyrocytes derived from individual patients allowing repeated sampling to investigate the time progression of the chronic disease or the effect of treatment over time.
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PMID:Isolation of thyroid cells obtained by fine-needle aspiration biopsy. 1618 6

The uptake of iodide represents the first step in thyroid hormone synthesis by thyroid follicular cells and is mediated by the sodium-iodide symporter (NIS). In mammals, expression of NIS is stimulated by TSH and transcription of the NIS gene involves regulation by the thyroid-specific transcription factors Pax8 and Nkx2.1. In this study, we examined the mRNA expression of NIS, Pax8 and Nkx2.1 in the thyroid gland of Xenopus laevis tadpoles by semi-quantitative reverse transcriptase (RT)-PCR. During spontaneous metamorphosis, NIS mRNA expression was low in premetamorphic tadpoles, increased throughout prometamorphosis, and peaked at climax stage 60. Analysis of TSH beta-subunit (TSHbeta) mRNA in the pituitary of the same tadpoles revealed a close temporal relationship in the expression of the two genes during metamorphosis, suggesting a regulatory role of TSH in the developmental expression of NIS. Treatment of tadpoles with goitrogenic compounds (sodium perchlorate and ethylenethiourea) increased TSHbeta mRNA expression (approximately twofold) and caused thyroid gland hyperplasia, confirming that feedback along the pituitary-thyroid axis was operative. Analysis of gene expression in the thyroid gland revealed that goitrogen treatment was correlated with increased expression of NIS mRNA (approximately 20-fold). In the thyroid gland organ culture experiments, bovine TSH (bTSH; 1 mU/ml) strongly induced NIS mRNA expression. This effect was mimicked by co-culture of thyroid glands with pituitaries from stage 58 tadpoles and by agents that increase intracellular cAMP (forskolin, dibutyryl-cAMP). In addition, it could be shown that thyroid glands of X. laevis tadpoles express Pax8 and Nkx2.1 mRNA in a developmentally regulated manner and that ex vivo treatment of thyroid glands with bTSH, forskolin, and cAMP analogs increased the expression of Pax8 and Nkx2.1 mRNA. This is the first report on developmental profiles and hormonal regulation of thyroid gland gene expression in amphibian tadpoles and, together, results reveal a critical role of TSH in the regulation of NIS mRNA expression in the thyroid gland of X. laevis tadpoles.
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PMID:Expression of sodium-iodide symporter mRNA in the thyroid gland of Xenopus laevis tadpoles: developmental expression, effects of antithyroidal compounds, and regulation by TSH. 1683 20

A full-length transcript encoding a functional lamprey glycoprotein hormone receptor I (lGpH-R I, GenBank AY750688) was cloned from the testes of the sea lamprey, Petromyzon marinus, using the GpH-R protein fingerprint GLYCHORMONER from the PRINTS database. The present study is the first to identify a GpH-R transcript in an agnathan, which is one of the only two representatives of the oldest lineage of vertebrates. The 719-amino acid full-length cDNA encoding lGpH-R I is highly similar and is likely a homolog of the vertebrate GpH-Rs (including LH, FSH, and TSH receptors). The key motifs, sequence comparisons, and characteristics of the identified GpH-R reveal a mosaic of features common to all other classes of GpH-Rs in vertebrates. The lGpH-R I was shown to activate the cAMP signaling system using human chorionic gonadotropin in transiently transfected COS-7 cells. The highest expression of the receptor transcript was demonstrated in the testes using reverse transcriptase-PCR. Lower levels of the receptor transcript were also detected in brain, heart, intestine, kidney, liver, muscle, and thyroid. The high expression of lGpH-R I in the testis and the high similarity with gnathostome gonadotropin hormone receptors suggest that lGpH-R I functions as a receptor for lamprey gonadotropin hormones. We hypothesize from these data that there is lower specificity of gonadotropin and its receptor in agnathans and that during co-evolution of the ligand and its receptor in gnathostomes, there were increased specificities of interactions between each GpH (TSH, LH, and FSH) and its receptor.
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PMID:Identification and cloning of a glycoprotein hormone receptor from sea lamprey, Petromyzon marinus. 1690 30


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