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)

Small-cell lung cancer (SCLC) synthesises a wide range of neuropeptides and their corresponding receptors. Together, these can form autocrine growth loops. Non-small-cell lung cancer (NSCLC) does not generally share this neuroendocrine phenotype. In this study, we tested the hypothesis that multiple neuropeptides and their receptors are co-expressed in SCLC, constituting potential autocrine loops. Expression of mRNA for arginine vasopressin, gastrin, cholecystokinin, gastrin-releasing peptide, endothelin and neurotensin, together with their cognate receptors, was evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) in a panel of human lung cancer cell lines. We have assessed those neuropeptides and neuropeptide receptors that could be used as potential early markers to detect lung cancer cells both as micrometastases in blood and within dysplasia in bronchial biopsies. We establish that although no cell line expressed all neuropeptides, co-expression of neuropeptides and their receptors is common in SCLC but not in NSCLC. We conclude that mRNA for the neuropeptides gastrin-releasing peptide and arginine vasopressin and the cholecystokinin receptor B were most SCLC-specific and RT-PCR for these markers could be used to distinguish between SCLC and NSCLC.
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PMID:Use of RT-PCR to detect co-expression of neuropeptides and their receptors in lung cancer. 1142 90

Previous studies showed that aquaporin 2 (AQP2) is elevated in the kidney of the heart failure rat suggesting that an increased amount of AQP2 contributes to water retention in heart failure. We performed the present study to determine whether angiotensin II play a role in causing an increase in the expression of arginine vasopressin (AVP) V2 and AQP2 mRNA in the kidney of the cardiomyopathic hamster. The expression of AVP V2 and AQP2 mRNA in the inner medullary collecting duct (IMCD) was measured by competitive reverse transcriptase-polymerase chain reaction (RT-PCR) before and after treatment with an angiotensin-converting enzyme inhibitor, enalapril. Our results showed that the expression of AVP V2 (0.53 +/- 0.05 v 1.03 +/- 0.15 amol/microg of total RNA, P <.01) and AQP2 mRNA (0.027 +/- 0.002 v 0.036 +/- 0.002 amol/microg of total RNA, P <.05) in the IMCD of the cardiomyopathic hamster is upregulated. Treating the cardiomyopathic hamster with enalapril for 7 days negated the changes. In situ hybridization experiments confirmed the intensity of the signals for both AVP V2 and AQP2 mRNA was more intense in the IMCD of the cardiomyopathic hamster. Enalapril treatment reduced the signal intensity to a level comparable to the normal hamster. These results suggested that the increases in the expression of AVP V2 and AQP2 mRNA are mediated by angiotensin II.
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PMID:Upregulation of vasopressin V2 and aquaporin 2 in the inner medullary collecting duct of cardiomyopathic hamsters is attenuated by enalapril treatment. 1214 68

Previous studies revealed that chronic (days) vasopressin treatment stimulates amiloride-sensitive sodium transport in isolated renal cortical collecting ducts and increases the abundance of beta- and gamma-subunits of the epithelial sodium channel (ENaC) in the kidney. The aim of the present work was to investigate in vivo the cellular basis of these effects. The long-term effect of V2 vasopressin agonist (1-deamino-8-D-arginine vasopressin (dDAVP)) on the abundance and subcellular localization of ENaC along the rat renal collecting system was determined by immunohistochemistry and laser confocal microscopy. Moreover, we studied by real-time reverse transcriptase-polymerase chain reaction the effect of vasopressin on proteins implicated in the regulation of ENaC (Nedd4-2, prostasin, Sgk1). After 5 days of administration, dDAVP markedly increased the intracellular pool of the beta- and gamma-ENaC subunits in the principal cells, with an increasing gradient from connecting tubule to the outer medullary collecting duct, but did not increase any subunit at the cell surface. The apical immunostaining of ENaC increased in response to sodium restriction, as expected, but dDAVP did not further enhance this apical labelling. dDAVP increased the gene expression of prostasin in the cortex but not that of Nedd4-2 and Sgk1. These findings suggest that the previously reported increase in sodium transport induced by sustained stimulation of vasopressin V2 receptor is probably mediated by other mechanism than an increase in the apical density of ENaC.
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PMID:Long-term effects of vasopressin on the subcellular localization of ENaC in the renal collecting system. 1652 52

In this study, the P2X(5) receptor was found to be distributed widely in the rat hypothalamus using single and double labeling immunofluorescence and reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The regions of the hypothalamus with the highest expression of P2X(5) receptors in neurons are the paraventricular and supraoptic nuclei. The intensity of P2X(5) immunofluorescence in neurons of the ventromedial nucleus was low. 70-90% of the neurons in the paraventricular nucleus and 46-58% of neurons in the supraoptic and accessory neurosecretory nuclei show colocalization of P2X(5) receptors and arginine vasopressin (AVP). None of the neurons expressing P2X(5) receptors shows colocalization with AVP in the suprachiasmatic and ventromedial nuclei. 87-90% of the neurons in the lateral and ventral paraventricular nucleus and 42-56% of the neurons in the accessory neurosecretory, supraoptic and ventromedial nuclei show colocalization of P2X(5) receptors with neuronal nitric oxide synthase (nNOS). None of the neurons expressing P2X(5) receptors in the suprachiasmatic nucleus shows colocalization with nNOS. These findings provide a morphological basis for possible functional interactions between the purinergic and nitrergic or vasopressinergic neurotransmitter systems.
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PMID:P2X5 receptors are expressed on neurons containing arginine vasopressin and nitric oxide synthase in the rat hypothalamus. 1676 18

Recent studies in our laboratory have demonstrated that angiotensin (ANG) II and endothelin (ET) 1 up-regulate the expression of arginine vasopressin V(2) receptor in the inner medullary collecting duct (IMCD) of the rat. The present studies were performed to explore the interaction between ANG II and ET-1 in up-regulating the expression of arginine vasopressin V(2) receptor in the IMCD of the rat. Two sets of studies were done. In the first set of studies, rat IMCD tissue was isolated and incubated with ANG II in combination with ET(A) or ET(B) antagonist. In the second set of experiments, rat IMCD tissue was incubated with ET-1 with ANG receptor antagonist saralasin. Tissue samples were then analyzed by means of quantitative reverse transcriptase polymerase chain reaction and Western blotting. The ANG II treatment resulted in increased V(2) messenger RNA (mRNA) from control level of 138 +/- 12 amol/microg of total RNA to 385 +/- 63 amol/microg of total RNA (P < .01). The ANG II/ET(A) treatment resulted in no significant decrease in V(2) mRNA expression (319 +/- 59 amol/microg of total RNA), whereas ET-1/ET(B) antagonist and ET-1/ET(A)/ET(B) antagonist treatments resulted in reducing V(2) mRNA to control levels of 214 +/- 25 and 176 +/- 22 amol/microg of total RNA, respectively. The ET-1 treatment increased V(2) mRNA expression from control level of 221 +/- 25 amol/microg of total RNA to 383 +/- 43 amol/microg of total RNA (P < .02). The ET-1-induced increase in V(2) mRNA expression was significantly reduced to control level (210 +/- 36 amol/microg of total RNA) after saralasin treatment. Western blotting revealed that changes in protein expression in the different treatment conditions were comparable with changes in V(2) mRNA expression. These data suggested that the up-regulation of V(2) receptor induced by ANG II and ET-1 is mediated by both vasoconstricting hormones. These 2 systems interact in up-regulating the expression of V(2) receptors in the kidney.
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PMID:Interaction between endothelin and angiotensin II in the up-regulation of vasopressin messenger RNA in the inner medullary collecting duct of the rat. 1788 47

Body fluid balance requires the release of arginine vasopressin (AVP) from the neurohypophysis. The hypothalamic supraoptic nucleus (SON) is one of the major sites for the synthesis of AVP, and secretion of AVP is controlled by the electrical activities of magnocellular neurosecretory cells (MNCs), which in turn are regulated by neuronal excitatory glutamatergic and inhibitory GABAergic inputs and humoral factors such as plasma osmolality. Previous studies have shown that brain-derived neurotrophic factor (BDNF) mRNA was increased by osmotic stress in the rat SON. In the present study, the effects of BDNF on excitatory and inhibitory synaptic inputs were examined in the MNCs of rat SON, using the whole-cell patch-clamp technique in in vitro brain slice preparations. BDNF application caused a significant reduction in the frequency and amplitude of the spontaneous inhibitory postsynaptic currents of the MNCs without affecting the spontaneous excitatory postsynaptic currents. Next, whole-cell patch-clamp recordings from dissociated SON MNCs expressing AVP-enhanced green fluorescent protein (eGFP) transgene revealed that the amplitude of GABA-induced currents were significantly smaller after BDNF treatment. Moreover, multi-cell reverse transcriptase-polymerase chain reaction (RT-PCR) experiments revealed the expression of TrkB mRNA in AVP-eGFP neurons. These results suggest that BDNF in the rat SON may decrease the postsynaptic GABAergic activity and may be involved in the regulatory mechanisms of body fluid homeostasis.
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PMID:Brain-derived neurotrophic factor inhibits spontaneous inhibitory postsynaptic currents in the rat supraoptic nucleus. 1915 Apr 37

Nociceptin/orphanin FQ (N/OFQ) peptide and its receptor (NOP) function in the neuromodulation of anxiety, stress and hypothalamic-pituitary-adrenal (HPA) axis activity. We investigated the endogenous NOP system using the selective NOP antagonist, UFP-101, during the HPA axis response to bacterial endotoxin, lipopolysaccharide (LPS). Although i.c.v. N/OFQ (1 microg/rat) had no significant effect on LPS-induced (250 microg/rat i.p) plasma corticosterone release at 30 or 60 min post-i.c.v. injection, i.c.v. UFP-101 (1 microg/rat)/LPS significantly attenuated plasma adrenocorticotrophic hormone and corticosterone at the 30-min time-point compared to i.c.v saline (0.9%)/LPS. Parvocellular paraventricular nucleus (PVN) corticotrophin-releasing factor (CRF) and corticotrophic pro-opiomelanocortin (POMC), but not parvocellular PVN arginine vasopressin (AVP), mRNA expression was significantly increased by LPS compared to non-LPS control. Intracerebroventricular UFP-101/LPS treatment was associated with increased POMC mRNA expression 4 h after injection and a clear trend towards increased parvocellular CRF mRNA. Furthermore, i.c.v. UFP-101 was selectively associated with an LPS-induced increase in parvocellular AVP mRNA, an effect that was absent in the i.c.v saline/LPS group. To determine whether LPS challenge was associated with compensatory changes in N/OFQ precursor or NOP receptor mRNAs, in a separate study, we undertook reverse transcriptase-polymerase chain reaction analysis of preproN/OFQ and NOP transcripts. In support of an endogenous role for central N/OFQ in inflammatory stress, we found that LPS significantly increased preproN/OFQ transcript expression in the hypothalamus 4 h after injection compared to the saline control. No changes in preproN/OFQ mRNA level in the hippocampus or basal forebrain (including bed nucleus of stria terminalis) were seen, albeit at 4 h. LPS was associated with a significant attenuation of NOP mRNA in the basal forebrain at 4 h, possibly as a compensatory response to increased N/OFQ release. Although the exact mechanisms require elucidation, the findings obtained in the present study provide evidence indicating that the endogenous NOP system is involved in the acute HPA axis response to immune challenge.
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PMID:Endogenous nociceptin / orphanin FQ system involvement in hypothalamic-pituitary-adrenal axis responses: relevance to models of inflammation. 1973 91

(Pro)renin receptor [(P)RR], a specific receptor for renin and prorenin, is a 350 amino acid protein with a single transmembrane domain. In the present study, the expression of (P)RR in the human brain and pituitary, and its co-localisation with arginine vasopressin and oxytocin in the human hypothalamus were studied by quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry. Human brain and pituitary tissues were obtained at autopsy from the subjects without neurological or endocrinological disorders. The antiserum against (P)RR was raised in a rabbit by injecting the peptide fragment of human (P)RR corresponding to 224-237 amino acids conjugated with bovine serum albumin. Quantitative RT-PCR showed that (P)RR mRNA was widely expressed in every region of brain examined and pituitary, with the highest expression levels found in the pituitary and frontal lobe. Immunocytochemistry showed that (P)RR was expressed in the paraventricular and supraoptic nuclei of human hypothalami, and in anterior pituitary cells. Immunostaining of serial sections showed that (P)RR was co-localised with arginine vasopressin and oxytocin in the magnocellular neurones of the paraventricular and supraoptic nuclei. The preabsorption of the antibody by the antigen peptide abolished the immunostaining of (P)RR in the human hypothalamus. The present study has shown that (P)RR mRNA is widely expressed in the human brain and pituitary, consistent with the hypothesis that (P)RR is related to the various brain functions, such as cognitive function and brain development. Co-localisation of (P)RR with vasopressin in the hypothalamus raised the possibility that (P)RR may be related to the central control of water-electrolyte metabolism and blood pressure.
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PMID:Expression of (pro)renin receptor in the human brain and pituitary, and co-localisation with arginine vasopressin and oxytocin in the hypothalamus. 2016 18

Body fluid balance requires the release of arginine vasopressin (AVP) from the neurohypophysis. The hypothalamic supraoptic nucleus (SON) is a major site of AVP synthesis, and AVP release is controlled somatodendritically or at the level of nerve terminals by electrical activities of magnocellular neurosecretory cells (MNCs). Acid-sensing ion channels (ASICs) are neuronal voltage-insensitive cationic channels that are activated by extracellular acidification. Although ASICs are widely expressed in the central nervous system, functional ASICs have not been assessed in AVP neurons. ASICs are modulated by lactate (La(-)), which reduces the extracellular calcium ion concentration. We hypothesize that ASICs modify neuronal function through La(-) that is generated during local hypoxia resulting from osmotic stimulation in the SON. In the present study, we used the whole-cell patch-clamp technique to show that acid-induced ASIC current is enhanced by La(-) in isolated rat SON MNCs that express an AVP-enhanced green fluorescent protein (eGFP) transgene. Immunohistochemistry and multi-cell reverse transcriptase-polymerase chain reaction experiments revealed that these neurons express the ASIC1a and ASIC2a subunits. In addition, increased La(-) production was specifically observed in the SON after osmotic stress. These results suggest that interaction between ASICs and La(-) in the SON plays an important role in the regulatory mechanism of body fluid homeostasis.
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PMID:Acid-sensing ion channels in rat hypothalamic vasopressin neurons of the supraoptic nucleus. 2044 65

Release of arginine vasopressin (AVP) from magnocellular neurosecretory cells (MNCs) of the supraoptic nucleus (SON) is controlled by the electrical activity of these neurons. ATP plays a crucial role in the regulation of SON MNCs by activating the purinergic P2X and P2Y receptors. Recent reports of interaction between P2X receptors and pannexin channels have provided new insights into the physiology of the central nervous system; however, the function of pannexin channels has not been assessed in AVP neurons. In the present study, we examined the possible contribution of the pannexin channel in ATP-induced responses in SON AVP neurons. We used the whole-cell patch-clamp technique in isolated rat SON MNCs that express an AVP-enhanced green fluorescent protein transgene. The ATP-induced current was inhibited in a concentration-dependent manner by pannexin channel blockers carbenoxolone and mefloquine, whereas the connexin channel blockers flufenamic acid and lanthanum had no effect. Multi-cell reverse transcriptase-polymerase chain reaction experiments confirmed the existence of pannexin-1 mRNA in AVP neurons. The involvement of the ATP-activated transient receptor potential vanilloid and acid-sensing ion channels was excluded. These results suggest that pannexin channels in SON AVP neurons are involved in the regulatory mechanisms of neuronal activity.
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PMID:Possible contribution of pannexin channel to ATP-induced currents in vitro in vasopressin neurons isolated from the rat supraoptic nucleus. 2153 56


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