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)

A chronic increase in systemic levels of acute-phase reactants contributes to the development of insulin resistance and associated disorders such as cardiovascular disease. Recently, serum amyloid A3 (SAA3) has been characterized as an adipocyte-secreted acute-phase reactant, expression of which is dramatically increased in insulin resistance and obesity. To further clarify expression and regulation of this adipocytokine in fat, SAA3 mRNA was measured by quantitative real-time reverse transcriptase PCR during differentiation of 3T3-L1 adipocytes and after treatment with various hormones known to induce insulin resistance and contribute to atherosclerosis. SAA3 mRNA was dramatically induced up to 77-fold during differentiation of 3T3-L1 preadipocytes. Furthermore, 100 nM dexamethasone and 30 ng/ml interleukin (IL)-6 induced SAA3 mRNA by up to 11- and 4.8-fold, respectively, in a time-dependent fashion with significant stimulation observed at concentrations as low as 10 nM dexamethasone and 1 ng/ml IL-6. In contrast, insulin, isoproterenol and growth hormone did not influence SAA3 synthesis. Inhibitor studies suggested that the positive effect of IL-6 on SAA3 expression is at least in part mediated by Janus kinase 2. Taken together, our results show a differential regulation of SAA3 by glucocorticoids and IL-6 supporting an integrative role of this acute-phase reactant in the pathogenesis of insulin resistance and its link to obesity and cardiovascular disease.
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PMID:Serum amyloid A3 expression is stimulated by dexamethasone and interleukin-6 in 3T3-L1 adipocytes. 1559 Sep 82

Extrapituitary expression of the growth hormone (GH) gene has been reported for the immune system of various vertebrates. In the rainbow trout (Oncorhynchus mykiss), GH mRNA could be detected in several lymphoid organs and leucocytes by reverse transcriptase-polymerase chain reaction (RT-PCR). To understand the control of GH expression in the fish immune system, mRNA levels for two distinct GH genes (GH1 and GH2) in trout leucocytes isolated from peripheral blood were quantified using a real-time PCR method. Both GH mRNAs could be detected in trout leucocytes, although their levels were extremely low compared to those in pituitary cells. The levels of GH2 mRNA in leucocytes were several times higher than those of GH1, while no difference was observed between GH1 and GH2 mRNA levels in the pituitary. Administration of dibutyryl cyclic AMP and cortisol produced a significant elevation of GH mRNA levels in trout leucocytes, although the levels were unchanged by T3. GH1 and GH2 mRNA levels showed similarities in responses to those factors. The effect of cortisol on GH mRNA appears biphasic; a dose-depending elevation of GH gene expression was observed in leucocytes treated with cortisol at below 200 nM, however, cortisol had no effect at 2000 nM. Cortisol-treated leucocytes showed no significant change in the mRNA level of beta-actin or proliferative activity during the experiments. Our results thus show that, at the low levels, GH gene expression in trout leucocytes is regulated by cortisol, which has been known as a regulatory factor of GH gene expression in pituitary cells, and suggest a physiological significance of paracrine GH produced in the fish immune system.
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PMID:Cortisol stimulates growth hormone gene expression in rainbow trout leucocytes in vitro. 1586 70

In the present study, the gene encoding hepatic glucose-6-phosphate dehydrogenase (G6PDH) was cloned and characterized from silver sea bream (Sparus sarba). The deduced amino acid sequence from sea bream g6pdh shared 78-84% homology with deduced amino acid sequences from previously cloned teleost g6pdh genes. A reverse transcriptase polymerase chain reaction (RT-PCR) coupled with radioisotope hybridization method was used for assessment of g6pdh expression and it was found that administration of growth hormone to sea bream increased g6pdh transcript and G6PDH activity whereas injections of somatostatin decreased both of these parameters. It was also found that sea bream maintained at an isoosmotic salinity (12 ppt) and cold temperature (12 degrees C) displayed upregulated g6pdh expression and enhanced G6PDH activtity. The results from this study demonstrate that g6pdh expression can be mediated by both hormonal and environmental factors in teleosts.
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PMID:Expression studies on glucose-6-phosphate dehydrogenase in sea bream: effects of growth hormone, somatostatin, salinity and temperature. 1601 52

The high-mobility group A2 (HMGA2) gene has a critical role in benign tumors where it is frequently rearranged, and in malignant tumors, where it is overexpressed in the absence of structural modification of the HMGA2 locus. By previous fluorescence in situ hybridization (FISH) and reverse transcriptase PCR analyses on human prolactin-secreting pituitary adenomas we detected rearrangement of the HMGA2 gene and amplification of its native region associated with activated expression. These data indicated a role for the HMGA2 gene in the development of human pituitary prolactinomas, since they are consistent with the appearance of prolactin/growth hormone adenomas in transgenic mice overexpressing the HMGA2 gene. To assess a more general role for HMGA2 in pituitary oncogenesis, we investigated HMGA2 amplification and expression in a panel of non-functioning pituitary adenomas (NFPAs) which account for 25% of all pituitary adenomas. We provide evidence that out of 18 NFPA tumors tested, 12 expressed HMGA2, but, different from prolactinomas, only in two cases the upregulation of the gene could be associated with amplification and/or rearrangement of the HMGA2 locus. Increased dosage of chromosome 12 was found in the expressing and non-expressing NFPAs, confirming that this sole event is insufficient to drive up activation of the HMGA2 gene. A role for chromosome 12 polysomy to promote structural instability of HMGA2 is confirmed, but the mechanism via trisomy is less prevalent in the frequently diploid NFPAs than in the usually hyperdiploid prolactinomas. Micro-rearrangements of HMGA2 gene not detectable by FISH analysis and/or sequence alterations could contribute to upregulation of HMGA2 gene in pituitary adenomas of the NFPA subtype. However, it cannot be excluded that the HMGA2 overexpression may be due, in some NFPA patients, to the same, still mainly unknown, mechanisms responsible for HMGA2 overexpression in malignant neoplasias.
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PMID:High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy. 1632 27

Recent studies have indicated that ghrelin stimulates growth hormone release from the pituitary via the growth hormone secretagogue receptor (GHSR). We have previously isolated two GHSR subtypes from the pituitary of the black seabream Acanthopagrus schlegeli. In the present study, we have cloned and characterized ghrelin from the same fish species at both the cDNA and gene levels. The full-length seabream ghrelin cDNA, isolated from sea-bream stomach using a novel approach by exploiting a single conserved region in the coding region, was found to encode a prepropeptide of 107 amino acids, with the predicted mature ghrelin peptide consisting of 20 amino acids (GSSFLSPSQKPQNRGKSSRV). Embedded in this full-length cDNA is a putative fish orthologue of the recently reported mammalian obestatin peptide. The ghrelin gene in black seabream, obtained by genomic PCR, was found to encompass four exons and three introns, possessing the same structural organization as in tilapia and goldfish, but different from that in rainbow trout. In addition, a 2230-bp 5'-flanking region of the seabream ghrelin gene was obtained by genome walking. Sequence analysis revealed that, as in the case of the human ghrelin gene, there is neither a GC box nor a CAAT box present in the isolated 5'-flanking region. However, a number of putative transcription factor-binding sites different from the human counterpart were found in the 5'-flanking region of the seabream ghrelin gene, suggesting that different cis- and trans-acting elements are involved in controlling their gene expression. Functional activity of this 5'-flanking region was examined by cloning it into the pGL3-Basic vector upstream of the luciferase reporter gene and transfected into various cell lines. Positive promoter activity could only be recorded in the colon-derived Caco-2 cells, suggesting that the cloned 5'-flanking region represents the functional promoter of the seabream ghrelin gene, which exhibits tissue-specific promoter activity. Using reverse transcriptase PCR analysis, expression of ghrelin was detected only in the seabream stomach, but not in the other tissues examined, including the brain, gill, intestine, kidney, liver and spleen. This stomach-specific expression of ghrelin in seabream is subject to regulation, as administration of growth hormone or ipamorelin to the fish in vivo was demonstrated to enhance its expression. Reminiscent of the homologous upregulation found in the transcriptional control of the seabream GHSR gene, a similar homologous regulatory mechanism might also exist in controlling the expression of seabream ghrelin. The identification of both GHSR and ghrelin from a single fish species would facilitate our subsequent studies on the elucidation of the physiological functions of the ghrelin/GHSR system in teleost. The possible existence of obestatin in teleost opens up new research avenues on the somatotropic axis in fish.
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PMID:Seabream ghrelin: cDNA cloning, genomic organization and promoter studies. 1664 3

Intrauterine growth restriction (IUGR) is one of the major causes of short stature in childhood. Abnormalities in the growth hormone (GH) axis have frequently been observed in children who are born intrauterine growth restricted and GH treatment is effective to improve final height. However, the way that the GH axis is involved is not fully understood. Previously, when investigating the effect of IUGR on the central somatotrophic axis, a hypothalamic effect was discovered with elevated somatostatin and decreased neuropeptide Y mRNA expression levels, whereas serum GH and insulin-like growth factor I (IGFI) were unaltered. These findings were thought to indicate a hypothalamic alteration of the GH axis due to IUGR, probably to compensate pituitary output, thereby normalising peripheral values of GH and IGFI. Therefore, the present study aimed to evaluate the effect of IUGR on the pituitary GH axis in this rat model. Pups from rats that underwent bilateral uterine artery ligation at day 17 of pregnancy were studied. Pituitary glands were collected from 1-year-old offspring for quantitative measurements of GH, GH-receptor (GH-R), GH-releasing hormone receptor (GHRH-R), somatostatin receptor subtype 2 and 5, IGFI and IGFI receptor mRNA levels using a real-time reverse transcriptase-polymerase chain reaction. In addition, liver GH-R and IGFI mRNA expression levels were measured and a radioimmunoassay was performed to determine serum IGFI levels. In the IUGR rat, levels of pituitary GH, GH-R and GHRH-R relative gene expression (RGE) were increased. No differences were found in the RGE level of all other pituitary growth factors, liver GH-R and IGFI, and serum IGFI concentration between IUGR and control rats. The present data show that intrauterine growth failure leads to changes in the pituitary that might counterbalance the effects found previously in the hypothalamus.
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PMID:Pituitary mRNA expression of the growth hormone axis in the 1-year-old intrauterine growth restricted rat. 1686 82

A cerebral growth hormone axis is activated following brain injury in the rat and treatment with growth hormone is neuroprotective. We have now investigated whether the closely related prolactin axis has similar properties following injury to the developing rat brain. From one day following a unilateral hypoxic ischemic injury, prolactin immunoreactivity was increased in the affected cortex parallel to the development of the injury (P<0.001). Initial prolactin and prolactin receptor staining on penumbral neurons progressively decreased whereas astrocytes remained strongly immunopositive. Reactive microglia also became strongly prolactin immunoreactive. Unlike growth hormone, central treatment with prolactin failed to rescue neurons in this paradigm. This was confirmed in vitro; rat prolactin failed to protect neurons under conditions for which growth hormone was neuroprotective. However, prolactin had trophic and pro-proliferative effects on glia (P<0.001). We confirmed the expression of the prolactin receptor in vitro by reverse transcriptase polymerase chain reaction, and show its strong association with astrocytes as compared with neurons by immunocytochemistry. In summary, we show for the first time that hypoxia ischemia induces a robust activation of the prolactin axis in regions of the cerebral cortex affected by injury. The lack of neuroprotective properties in vivo and in vitro indicates that, unlike growth hormone, prolactin is not directly involved in neuronal rescue in the injured brain. Its strong relation to glial reactions and its gliatrophic effects suggest that the prolactin axis is primarily involved in a gliogenic response during recovery from cerebral injury.
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PMID:Prolactin is involved in glial responses following a focal injury to the juvenile rat brain. 1731 19

The pituitary is the central organ regulating virtually all endocrine processes, and pathologies of the pituitary cause manifold adverse effects. Because insulin-like growth factor (IGF)-I appears to be involved in tumour pathogenesis, progression, and persistence, and only few data exist on the cellular synthesis sites of IGF-I, the present study aims to create a basis for further research on pituitary adenomas by investigating the presence of IGF-I in the human pituitary using reverse transcriptase-polymerase chain reaction, in situ hybridisation, immunohistochemistry and immunocytochemistry. IGF-I was expressed in the pituitary, and gene sequence analysis revealed a sequence identical to that found in human liver. The distribution pattern of IGF-I mRNA found by in situ hybridisation corresponded to that of IGF-I peptide in immunohistochemistry. In all pituitary samples investigated, IGF-I-immunoreactivity occurred in almost all adrenocorticotrophic hormone (ACTH)-immunoreactive cells. Occasionally, an interindividually varying number of growth hormone (GH) and, infrequently, follicle-stimulating hormone and luteinising hormone cells contained IGF-I-immunoreactivity but none was detected in supporting cells. At the ultrastructural level, IGF-I-immunoreactivity was confined to secretory granules in coexistence with ACTH- or GH-immunoreactivity, respectively, indicating a concomitant release of the hormones. Thus, in humans, IGF-I appears to be a constituent in ACTH cells whereas its production in GH-producing and gonadotrophic cells may depend on the physiological status (e.g. serum IGF-I level, age or reproductive phase). It is assumed that locally produced IGF-I plays a crucial role in the regulation of endocrine cells by autocrine/paracrine mechanisms in addition to the endocrine route.
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PMID:Insulin-like growth factor-I mRNA and peptide in the human anterior pituitary. 1742 8

Fourteen-day-old rat pituitary tissue represents an attractive model for studying cell population dynamics, particularly of gonadotrophs. Prolonged three-dimensional culture in serum- and hormone-free medium causes a striking decline in somatotroph abundance but a several-fold rise in monohormonal LH beta-positive cell number, whereas bihormonal gonadotrophs almost disappear. In the present study, we investigated whether these changes are inter-related by examining the effects of growth hormone-releasing hormone (GHRH) and glucocorticoids, two protagonist regulators of somatotrophs. Cells were identified by single cell reverse transcriptase-polymerase chain reaction (RT-PCR) and immunofluorescence. Supplementation of the cultures for 2 weeks with GHRH (1 nm) did not augment the proportion of somatotrophs, but expanded the nonhormonal cell population. GHRH reduced the proportion of monohormonal luteinising hormone (LH)beta mRNA positive cells to approximately 50% of control, although the effect was not seen when these cells were visualised by immunostaining. Supplementation of the cultures with dexamethasone (4 nM) for 3 weeks partially rescued LH beta/follicle-stimulating hormone beta cells and fully rescued the GH mRNA cells in parallel with a decline in nonhormonal cell abundance, but strongly reduced bromodeoxyuridine labelling of GH-immunoreactive cells. As studied by patch-clamp single cell RT-PCR at the start of culture, GHRH caused an acute rise in intracellular [Ca(2+)] in some monohormonal GH cells, but at a higher incidence in cells expressing LH beta mRNA, alone or in combination with GH mRNA and/or pro-opiomelanocortin (POMC) mRNA. The present data suggest that, in the 14-day-old rat pituitary, the majority of GHRH target cells are cells expressing LH beta mRNA alone or in combination with GH and/or POMC mRNA. The data show co-regulation of gonadotroph and somatotroph population sizes by glucocorticoids and GHRH, with the former preserving bihormonal gonadotrophs and the latter repressing LH beta-only cell abundance. GHRH may not expand the somatotroph population unless glucocorticoid hormone is present to maintain terminal differentiation.
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PMID:Growth hormone-releasing hormone and glucocorticoids determine the balance between luteinising hormone (LH) beta- and LH beta/follicle-stimulating hormone beta-positive gonadotrophs and somatotrophs in the 14-day-old rat pituitary tissue in aggregate cell culture. 1836 7

Somatostatin (SS) and growth hormone-releasing hormone (GHRH) are synthesized and secreted by the hypothalamus, which can control the synthesis and secretion of the growth hormone (GH) from the hypophysis as well as regulate the GH concentrations in animals and humans. In this article, we describe the regulation of animal growth using plasmid DNA encoding both the GHRH gene and the SS gene fused with the hepatitis B surface antigen (HBsAg) gene. We constructed a series of expression plasmids to express the GHRH and HBsAg-SS fusion genes individually as well as collectively. The fusion gene and GHRH were successfully expressed in Chinese hamster ovary (CHO) cells, as proven by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoblotting tests. Poly D, L-lactide-co-glycolic acid (PLGA) plasmid-encapsulating microspheres were prepared and injected intramuscularly into the leg skeletal muscles of rabbits. Weight gain/day and the levels of insulinlike growth factor-I (IGF-I), SS, and hepatitis B surface antibody (HBsAb) were monitored. During days 30 postinjection, increase in weight gain/day and IGF- I concentration and decrease in SS were observed in treatment groups. From days 15 to 30 postinjection, the weight gain/day significantly increased (P < 0.05) by 129.13%, 106.8%, and 72.82% relative to the control group in the co-expression GHRH and fusion gene (named P-G-HS), fusion gene (named P-HS), and GHRH (named P-G) groups, respectively. And most importantly, the P-G-HS group showed significant weight gain/day (P < 0.05) relative to the P-G and P-HS groups. A significant increase in the IGF-I concentration and decrease in the SS level relative to the control group were also observed. The results indicated that the combination of plasmid-mediated GHRH supplementation and positive immunization against SS led to more robust weight gain/day in rabbits.
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PMID:Simultaneous expression of growth hormone releasing hormone (GHRH) and hepatitis B surface antigen/somatostatin (HBsAg/SS) fusion genes in a construct in the skeletal muscle enhances rabbit weight gain. 1843 1


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