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)

Previous research has reported that elevations in circulating growth hormone (GH) levels in meat-type chickens depresses feed intake (FI) more than 30%. It is known that the product of the obese gene, leptin, functions to regulate FI and energy expenditure. To investigate the effect of GH on leptin gene expression, broiler chickens were infused with recombinant chicken GH. To separate any secondary effects of a GH-induced reduction in FI on leptin expression, groups of birds were pair-fed to an average level of voluntary intake similar to GH-treated birds, but received no GH treatment. GH treatment induced a dose-dependent increase in liver leptin gene expression, as measured by reverse transcriptase-polymerase chain reaction, whereas leptin expression in adipose tissue was unchanged. Conversely, in chickens pair-fed (feed-restricted) there was a decrease in leptin gene expression in both tissues. These results provide evidence of a direct effect of GH on leptin gene expression, which is independent of any effects on intake attributable to GH-treatment, and suggest differential regulation of leptin expression between adipose tissue and liver. The results of these experiments provide the first evidence of a relationship between GH and leptin in domestic birds.
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PMID:Effects of growth hormone and pair-feeding on leptin mRNA expression in liver and adipose tissue. 1048 32

The molecular mechanism of nitric oxide synthase (NOS)-containing nerve regeneration is still unknown. It is believed that growth factors are involved in this phenomenon. We investigated the change of NOS containing nerve fibers and the mRNA expression of insulin like growth factor (IGF)-I, nerve growth factor (NGF), transforming growth factor (TGF)-alpha, TGF-beta1, TGF-beta2, TGF-beta3, vascular endothelial growth factor (VEGF), endothelial NOS (eNOS) and neuronal NOS (nNOS) on the penis after cavernous nerve neurotomy in rats. Male rats were divided into four groups: (1) sham operation (n = 14); (2) unilateral neurotomy of a 5 mm segment of the cavernous nerve (n = 21); (3) unilateral neurotomy with growth hormone (n = 14); and (4) bilateral neurotomy (n = 21). Electrostimulation of the intact cavernous nerve or pelvic ganglion were performed at one, three and six months. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining and immunohistochemistry were used to identify NOS in the penis. The gene expression for growth factors, eNOS and nNOS were investigated in corporal tissue by reverse transcriptase-polymerase chain reaction (RT-PCR). One month after neurotomy, both unilateral and bilateral neurotomy groups showed significant decreases in NOS-containing nerve fibers on the dorsal and intracavernosal nerves on the side of neurotomy. Significantly lower mRNA expression of nNOS, IGF-I and TGF-beta2, higher mRNA expression of eNOS and VEGF189 were shown in these groups. At three months, the number of NOS-containing nerve fibers in the unilateral neurotomy group increased only slightly, while the GH-treated group showed a significant increase. At six months, those in the intracavernosal nerve only increased in a significant amount (P < 0.0001), however mRNA expression of nNOS, IGF-I and TGF-beta2 showed a significant increase as early as at three months. After bilateral neurotomy, the NOS-positive nerve fibers in the dorsal and intracavernosal nerve were significantly decreased at one month and remained so at six months; no erectile response could be elicited by pelvic ganglion stimulation. In the unilateral neurotomy group at six months, more NOS-positive neurons in the pelvic ganglia were found on the intact side than on the side of the neurotomy (P < 0.003), indicating that the regeneration derived from pelvic ganglion neurons on the intact side. Furthermore, electrostimulation in the unilateral neurotomy group revealed a greater maximal intracavernosal pressure and a shorter latency period at six months than at one month (P < 0.014, P < 0.001, respectively). These data suggest that IGF-I and TGF-beta2 may play a key role in the regeneration of nNOS-containing nerve fibers in the dorsal and intracavernosal nerves, and eNOS increases temporarily in the intracavernous involving VEGF189 after unilateral cavernous nerve injury.
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PMID:IGF-I and TGF-beta2 have a key role on regeneration of nitric oxide synthase (NOS)-containing nerves after cavernous neurotomy in rats. 1055 3

Linear bone growth occurs as the result of proliferation and differentiation of growth-plate chondrocytes. These two phases of chondrocyte growth are regulated separately, with insulin-like growth factor I (IGF-I) being the primary stimulator of proliferation. We studied the expression of the components of the growth hormone GH/IGF system to learn if this proliferative signal is altered as chondrocytes undergo differentiation. Growth-plate chondrocytes were isolated from fetal cows and fractionated on discontinuous Percoll gradients. Five populations were recovered, ranging from high density cells (proliferative chondrocytes) to low density cells (hypertrophic chondrocytes). Messenger RNAs (mRNAs) were analyzed by a reverse transcriptase/quantitative polymerase chain reaction (RT/qPCR) technique. Results showed that mRNA of IGF-I and IGF-II in proliferative chondrocytes was 32 and five fold more abundant, respectively, than in hypertrophic chondrocytes. Of the four major IGF-I mRNA transcripts, the class 1-Ea transcript was predominant. Messenger RNA levels for IGFBP-3, -4, and -5 were also reduced in hypertrophic chondrocytes. Levels of GH receptor, the type 1 IGF receptor, and IGF binding protein-2 (IGFBP-2) mRNAs were unchanged across the growth-plate. Since IGF-I and -II are potent stimulators of proliferation, the down-regulation of these genes may be necessary in order for hypertrophy to proceed.
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PMID:Expression of the components of the insulin-like growth factor axis across the growth-plate. 1061 24

The mud loach (Misgurnus mizolepis) growth hormone (GH) gene was cloned and a comparative analysis on its genomic organization was performed. Based on Southern analysis using various kinds of restriction endonucleases, the GH gene proved to exist as a single-copy gene in the mud loach. The complete nucleotide sequences of a 5.1 kb SacI/EcoRI genomic fragment containing the mud loach GH gene and its 5' flanking sequences as well as a mud loach GH cDNA obtained by rapid amplification of a reverse transcriptase-PCR have been determined. The GH gene spans 2.0 kb from the start codon to the polyadenylation signal, and contains five exons and four introns similar to those of carps and mammals. The evolutionary relation of the mud loach GH gene, inferred by comparative analyses of gene structures and sequences in each exon and intron of representative teleost GH genes, reflects the major phylogenetic groupings of teleost.
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PMID:Genomic organization and sequence of the mud loach (Misgurnus mizolepis) growth hormone gene: a comparative analysis of teleost growth hormone genes. 1067 31

ADP-ribosylation factors (ARFs) constitute a family of structurally related proteins that forms a subset of the Ras superfamily of regulatory GTP-binding proteins. Like other GTPases, activation of ARFs is facilitated by specific guanine nucleotide exchange factors (GEFs). In chromaffin cells, ARF6 is associated with the membrane of secretory granules. Stimulation of intact cells or direct elevation of cytosolic calcium in permeabilized cells triggers the rapid translocation of ARF6 to the plasma membrane and the concomitant activation of phospholipase D (PLD) in the plasma membrane. Both calcium-evoked PLD activation and catecholamine secretion in permeabilized cells are strongly inhibited by a synthetic peptide corresponding to the N-terminal domain of ARF6, suggesting that the ARF6-dependent PLD activation near the exocytotic sites represents a key event in the exocytotic reaction in chromaffin cells. In the present study, we demonstrate the occurrence of a brefeldin A-insensitive ARF6-GEF activity in the plasma membrane and in the cytosol of chromaffin cells. Furthermore, reverse transcriptase-polymerase chain reaction and immunoreplica analysis indicate that ARNO, a member of the brefeldin A-insensitive ARF-GEF family, is expressed and predominantly localized in the cytosol and in the plasma membrane of chromaffin cells. Using permeabilized chromaffin cells, we found that the introduction of anti-ARNO antibodies into the cytosol inhibits, in a dose-dependent manner, both PLD activation and catecholamine secretion in calcium-stimulated cells. Furthermore, co-expression in PC12 cells of a catalytically inactive ARNO mutant with human growth hormone as a marker of secretory granules in transfected cells resulted in a 50% inhibition of growth hormone secretion evoked by depolarization with high K(+). The possibility that the plasma membrane-associated ARNO participates in the exocytotic pathway by activating ARF6 and downstream PLD is discussed.
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PMID:Identification of a plasma membrane-associated guanine nucleotide exchange factor for ARF6 in chromaffin cells. Possible role in the regulated exocytotic pathway. 1074 97

Although effective treatment of antiretroviral-associated metabolic abnormalities ultimately depends on understanding the mechanisms involved, clinicians facing these problems are beginning to feel compelled to do something now to manage treatment-related metabolic complications. Diet and exercise should not be overlooked, because both can be effective in managing these complications without causing further side effects. Fibric acid derivatives such as gemfibrozil and statins can lower HIV-associated cholesterol and triglyceride levels, although further data are needed on problematic interactions between statins and protease inhibitors (PIs). Hypoglycemic agents may have some role in managing glucose abnormalities, although troglitazone cannot be recommended for fat abnormalities alone and metformin may cause lactic acidosis. Growth hormone and anabolic steroids may have some role in treating lipodystrophy, but the cost of growth hormone is prohibitive for many patients and definitive data on efficacy are lacking. Replacing a PI with a reverse transcriptase inhibitor has improved lipid and glucose levels in some studies. However, that strategy begs the question of how the nucleosides might contribute to lipodystrophy.
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PMID:How to manage metabolic complications of HIV therapy: what to do while we wait for answers. 1075 16

The structure of the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has been characterized in several species including protochordates, fish, amphibians, birds, and mammals. Although PACAP has been shown to stimulate frog pituitary and adrenal cell activity, the structure of the PACAP precursor and the expression of its gene have not yet been reported in any amphibian species. In this study, we have characterized two cDNA variants encoding PACAP of the frog Rana ridibunda, one of which encodes a second peptide exhibiting strong homologies to growth hormone-releasing hormone (GHRH) of fish and mammals. Northern blot and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses revealed that PACAP/GHRH-like peptide mRNAs are predominantly expressed in the brain and spinal cord and, to a lesser extent, in the neurointermediate lobe of the pituitary. Other tissues including the testis and the distal lobe of the pituitary do not express the PACAP precursor gene. The distribution of PACAP/GHRH-like peptide mRNAs in the frog brain has been determined by in situ hybridization histochemistry. High levels of expression were found in the accessory olfactory bulb, the distal pallium, the ventral part of the magnocellular preoptic nucleus, the ventral hypothalamic nucleus, the posterior tuberculum, and the ventral habenular nucleus. These data contribute to the understanding of the evolution of the PACAP and GHRH genes in vertebrates and provide the anatomical bases to elucidate the roles of PACAP and the GHRH-like peptide in amphibians.
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PMID:Structure and distribution of the mRNAs encoding pituitary adenylate cyclase-activating polypeptide and growth hormone-releasing hormone-like peptide in the frog, Rana ridibunda. 1081 84

Glucocorticoids regulate growth hormone (GH) secretion by modulating both hypothalamic and pituitary function. At the level of the pituitary, glucocorticoids increase GH and GH-releasing hormone receptor (GHRH-R) gene expression. To test if glucocorticoids might also regulate the pituitary expression of the recently identified GH secretagogue (GHS) receptor, GHS-R; adult male rats were adrenalectomized or sham operated, and treated with the synthetic glucocorticoid (dexamethasone, 200 microg/day) or vehicle for 8 days. Pituitary GHS-R mRNA levels were assessed by reverse transcriptase polymerase chain reaction (RT-PCR). Adrenalectomy decreased pituitary GHS-R mRNA to 45% of vehicle-treated, sham-operated rats (P < 0.05). Administration of dexamethasone increased GHS-R mRNA levels in sham-operated as well as in adrenalectomized rats (199 +/- 24% (P < 0.05) and 369 +/- 48% (P < 0.01) of vehicle-treated controls). Addition of dexamethasone to primary rat pituitary cell cultures increased GHS-R mRNA levels in a dose- and time-dependent manner while the transcriptional inhibitor, actinomycin D, completely blocked the stimulatory action of dexamethasone. Taken together, these results suggest glucocorticoids directly increase pituitary GHS-R mRNA levels by stimulating GHS-R gene transcription.
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PMID:Glucocorticoids regulate pituitary growth hormone secretagogue receptor gene expression. 1084 75

The potential effect of growth hormone (GH) in tumorigenesis, particularly in acute leukemia is controversial. Human growth hormone has the ability to influence certain immune functions; the majority of immune cells express growth hormone receptor (GHR) on plasma membranes. We determined GHR gene expression on different human lymphocyte (JURKAT, CESS) and monocyte (U937, THP1) cell lines by reverse transcriptase polymerase chain reaction analysis of GHR mRNA after stimulating the cells with phytohaemagglutinin or phorbolester, human growth hormone and with a combination of these. The receptor gene expression showed differences; in the U937 and CESS cell lines only the stimulants were able to induce GHR mRNA expression; in the case of JURKAT cells even the hormone alone had the ability to express its own receptor gene. Both the increased TNF-alpha production of U937 (but not that of THP1 cells), and the decreased proliferation of JURKAT cells in response to GH stimuli also prove the presence of biologically active GHR on the cell surface. Our data suggest asymmetric interaction between GH or phorbolester-induced signal pathways in U937 cells sharply depending on the temporal sequence of treatments. THP1 monocytes showed no gene expression in response to any of the stimulants. The phenomenon that certain human lymphoid and monocytoid cell lines at different levels of cell differentiation are able to express the GH receptor gene could have importance in the rhGH therapy.
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PMID:Growth hormone receptor gene expression on human lymphocytic and monocytic cell lines. 1087 96

In spite of the importance of IGF-I for growth and development, knowledge about regulation of its production in submammalian species is rather limited. In order to create a tool for investigation of direct regulatory effects on the expression of IGF-I in bony fish liver, a primary cell culture of hepatocytes from Oreochromis mossambicus, the tilapia, was established. The cells were viable for up to 3 days and IGF-I mRNA synthesis was detected by northern blot and semiquantitative reverse transcriptase (RT)-PCR. Northern blot analysis of the primary cultured hepatocytes revealed four different IGF-I transcripts, 0.5, 1.9, 3.9 and 6.0 kb in size, which were identical to those in liver tissue. However, the expression rate was weaker than that in liver. The direct effects of recombinant tilapia (rt) growth hormone (GH) and salmon (s) IGF-I on the expression of IGF-I in primary cultured hepatocytes were investigated in time-course and dose-response experiments. In untreated cultures, IGF-I mRNA decreased with time. Hepatocytes treated with 100 nM rtGH resulted in a pronounced stimulation of IGF-I mRNA expression throughout the experiment. Treatment with rtGH in concentrations ranging from 0.1 nM to 1 microM caused a clear dose-dependent increase in the amount of IGF-I mRNA. Significant stimulation was obtained even with 0.1 nM, reaching a plateau with 10 nM. Neither significant inhibitory nor stimulatory effects were detected by adding sIGF-I from 0.1 nM to 1 microM to the hepataocytes. Our results indicate that the established primary cell culture of tilapia hepatocytes is a useful system in which to study direct effects of potential regulators of bony fish liver cell function.
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PMID:Primary cultured hepatocytes of the bony fish, Oreochromis mossambicus, the tilapia: a valid tool for physiological studies on IGF-I expression in liver. 1092 16


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