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)

Aldosterone induces cardiac remodeling in cardiovascular diseases by stimulating the proliferation, production and secretion of collagen in fibroblasts. It also stimulates vascular smooth muscle cells to produce and secrete adrenomedullin (ADM), which has a cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion in rat cardiac fibroblasts, and the effect of ADM on aldosterone-stimulated fibroblast proliferation to observe the interaction between endogenous ADM and aldosterone. We detected ADM produced and secreted from cultured cardiac fibroblasts and the intracellular cAMP level by radioimmunoassay; evaluated cell proliferation by the level of [3H]-thymine incorporation; measured preproADM gene expression by reverse transcriptase polymerase chain reaction (RT-PCR); and monitored extracellular signal related kinase (ERK) activity by the phosphorylation of myelin basic protein in the presence of [gamma-32P] ATP. Our results showed that aldosterone-stimulated secretion of ADM and its mRNA expression were concentration-dependent, which could be inhibited by the specific antagonist of mineralocorticoid receptor, spironolactone. In contrast, ADM inhibited aldosterone-induced fibroblast proliferation and ERK activity. Treatment with ADM24-50 (a new antagonist of specific ADM receptors) and calcitonin gene-related peptide (CGRP)8-37 (the antagonist of CGRP receptor type 1), to attenuate the action of endogenous ADM, reinforced the aldosterone-induced proliferation and inhibited the intracellular cAMP production stimulated by aldosterone. Thiorphan, an inhibitor of ADM degradation, inhibited the [3H]-thymine incorporation and reinforced the intracellular cAMP level induced by aldosterone. We reach the conclusion that aldosterone stimulates rat cardiac fibroblasts to produce and secrete ADM, which in turn regulates the proliferation-induced effects of aldosterone in these cells.
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PMID:Effects of adrenomedullin on aldosterone-induced cell proliferation in rat cardiac fibroblasts. 1551 34

Recent evidence has shown calcitonin gene-related peptide (CGRP) to be a key mediator of stress-induced suppression of the gonadotrophin-releasing hormone (GnRH) pulse generator, although little is known about the neural pathways involved. In the present study, we investigated the potential direct action of CGRP on GnRH neurones using GT1-7 cells, an established GnRH cell line. First, we detected expression of the CGRP receptor subunits, calcitonin receptor-like receptor and receptor activity-modifying protein-1 in the GT1-7 cells by reverse transcriptase-polymerase chain reaction. Second, we have shown that CGRP inhibits GnRH mRNA expression in the GT1-7 cells, which was effectively reversed by the CGRP receptor antagonist, CGRP8-37. These results suggest that CGRP down regulates expression of GnRH mRNA, via CGRP receptors in the GT1-7 cell, thus implying that a potential direct action of CGRP may mediate a suppressive effect on the GnRH neural network.
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PMID:Effect of calcitonin gene-related peptide on gonadotrophin-releasing hormone mRNA expression in GT1-7 cells. 1610 91

Although a strong correlation between neuroendocrine differentiation and angiogenesis of prostate cancer has been reported, no mechanistic link between the two events has been established. Because neuropeptide calcitonin is secreted by prostate tumors and endothelial cells are known to express calcitonin receptor-like receptor, we examined the potential action of calcitonin on endothelial cells. The presence of calcitonin receptor, calcitonin receptor-like receptor, and receptor activity-modifying proteins in human microvessel endothelial-1 cells was tested by reverse transcriptase-PCR (RT-PCR). The proangiogenic action of calcitonin was examined in several in vitro models of angiogenesis using HMEC-1 cells and also in vivo using dorsal skinfold assays. Calcitonin expression of PC-3M cells was modulated, and its effect on angiogenesis was examined in in vitro as well as in vivo models. The results of RT-PCR and radioligand receptor assays showed the presence of functional calcitonin receptor in HMEC-1 cells. Calcitonin stimulated all phases of angiogenesis through the calcitonin receptor, but its effect on tube morphogenesis by endothelial cells occurred at the concentration of the Kd of calcitonin receptor. Silencing of calcitonin receptor expression in HMEC-1 cells abolished calcitonin-induced tube formation. Vascular endothelial growth factor antibodies attenuated but did not abolish calcitonin-induced tube morphogenesis. PC-3M prostate cancer cells induced angiogenesis in in vivo and in vitro models. Overexpression of calcitonin in PC-3M cells increased their angiogenic activity, whereas the silencing of calcitonin expression abolished it. These results show that prostate tumor-derived calcitonin may play an important role in prostate tumor growth by regulating intratumoral vascularization.
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PMID:Calcitonin stimulates multiple stages of angiogenesis by directly acting on endothelial cells. 1616 33

In avian species, the ultimobranchial anlage is populated with neuronal cells derived from the distal vagal ganglion. We found that ultimobranchial C cells of chick embryos cultured in the presence of nicotinamide continued to grow for at least 60 days and exhibited profound morphological changes, resulting in the formation of dense networks of neuronal fibers. Nicotinamide, thus, facilitated the manifestation of neuronal features in C cells. The neuronal phenotypes of cultured C cells were analyzed in detail by both scanning and transmission electron microscopy. Their neural nature was also positively established by immunostaining with monoclonal antibodies to the neuronal markers neuron-specific class III beta-tubulin (TuJ1), microtubule-associated protein (MAP) 2, and synaptophysin. Confocal laser scanning microscopy confirmed that these neuron-specific proteins are colocalized with calcitonin in both the somata and the neuronal processes of C cells. Furthermore, reverse transcriptase-polymerase chain reaction analyses, performed at various times up to 30 days in culture, indicated that the C cells have persistent gene expression of calcitonin, the catecholamine-synthesizing enzyme tyrosine hydroxylase, proenkephalin, proopiomelanocortin, neuron-specific beta-tubulin (cbeta4), SCG10, and Bcl-2. The morphological responses of C cells to nicotinamide treatment were analyzed quantitatively over a period of 60 days. The area of C-cell colonies, number of processes per colony, and length of processes continued to increase until culture day 45. In conclusion, nicotinamide stimulates long-term survival and neuronal differentiation of chick embryo C cells, and this culture system may provide a useful model for studying neuronal differentiation mechanisms.
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PMID:Nicotinamide promotes long-term survival and extensive neurite outgrowth in ultimobranchial C cells cultured from chick embryos. 1621 94

In this study we aimed to assess in vivo, the vasodilator effects of adrenomedullin, proadrenomedullin N-terminal 20 peptide (PAMP) and amylin in human skin vasculature and compare the responses to the effects mediated by the endogenous neuropeptides calcitonin gene-related peptide (CGRP) and substance P and to examine the mRNA expression of calcitonin receptor-like receptor (CL-R) and receptor-activity modifying proteins, RAMP1, RAMP 2 and RAMP3 in human subcutaneous arteries. Changes in skin blood flow of the forearm were measured using a Laser Doppler Imager after intradermal injection of the peptides. The mRNA expression was assessed by real-time reverse transcriptase-polymerase chain reaction (real-time PCR). CGRP, adrenomedullin and amylin induced concentration-dependent, long-lasting increases in skin blood flow. The response to PAMP was shorter in duration appearing similar to the transient response induced by substance P. PAMP (10(-6)-10(-5) M) caused distinct itch sensation and local erythema. This effect could be abolished when combining the histamine H1-receptor antagonist mepyramin and PAMP. Real-time PCR data showed a higher level of mRNA for RAMP2 than CL-R, RAMP1 and RAMP3 in the tissue. Though the PCR data demonstrated the presence of mRNA for both CGRP1 and adrenomedullin receptors the rank order of potency (CGRP>adrenomedullin>amylin) for the blood flow increase indicated vasodilatation for these peptides was induced by activation of CGRP1 receptors. Intradermal injection of CGRP, adrenomedullin and amylin induces long lasting dilatation of human skin vasculature by activation of CGRP1 receptors. PAMP induces transient vasodilatation. PAMP but not CGRP, adrenomedullin and amylin causes itch sensation and local erythema. The transient effect on vasodilatation as response to PAMP is discussed.
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PMID:The vasorelaxant effect of adrenomedullin, proadrenomedullin N-terminal 20 peptide and amylin in human skin. 1691 18

Recent data support an important role for calcitonin gene-related peptide (CGRP) in deep tissue nociceptive processing. Using real-time reverse transcriptase polymerase chain reaction (RT-PCR), radioimmunoassay, immunohistochemistry and behavioral testing, we studied the early time course of CGRP mRNA and protein expression as well as nociceptive behavior following muscle inflammation. A rapid and significant increase in CGRP mRNA occurred in the mandibular division (V3) of the ipsilateral trigeminal ganglion at 30 minutes, 4 and 24 h after the injection of complete Freund's adjuvant as an inflammatory agent into rat masseter muscle. No change in mRNA occurred in the ipsilateral ophthalmic and maxillary divisions (V1/V2) or in the contralateral V3. The levels of immunoreactive calcitonin gene-related peptide (iCGRP) in the ipsilateral V3 significantly increased at 1, 4 and 24 h following muscle inflammation. In contrast, no change occurred in iCGRP levels in either the ipsilateral V1/V2 or contralateral V3. When saline was injected into the masseter muscle, the levels of mRNA or iCGRP did not change in the ipsilateral V3 suggesting that the biochemical changes are specific to CFA-induced muscle inflammation. The number of muscle afferent neurons immunoreactive for CGRP was significantly reduced compared with control at 1, 4 and 24 h in the ipsilateral but not in the contralateral trigeminal ganglion following inflammation. This decrease in the ipsilateral ganglion may indicate a loss of intrasomatic CGRP as a result of increased axonal transport away from the neuronal cell body and/or release of CGRP. Behavioral testing showed a reduction in head withdrawal thresholds bilaterally from 30 min through 24 h following muscle inflammation. Thus upregulation of CGRP mRNA and iCGRP levels are temporally related to the development of inflammation and lowered pain thresholds. The present data support the hypothesis that CGRP is upregulated during deep tissue inflammation and suggest that gene transcription is involved in this upregulation.
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PMID:Muscle inflammation induces a rapid increase in calcitonin gene-related peptide (CGRP) mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior. 1702 65

Spinal cord injury (SCI) often results in intractable chronic central pain syndromes. Recently chemokines such as CCL2 were identified as possible key integrators of neuropathic pain and inflammation after peripheral nerve lesion. The focus of the current study was the investigation of time-dependent CCL2 and CCR2 expression in relation to central neuropathic pain development after spinal cord impact lesions of 100, 150, or 200 kdyn force on spinal cord level T9 in adult rats. Below-level pain was monitored with weekly sensory testing for 42 days after SCI. In parallel expression of CCL2/CCR2 on cervical, thoracic, and lumbar levels was investigated by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry early (7 days [7d]), intermediate (15d), and late (42d) after lesion. Cellular source and anatomical pain related expression was determined by double-immunohistochemistry. Force-defined SCI led to acute mechanical hypersensitivity in all lesion groups, and to persistent below-level pain in severely injured animals. While in the early post-operative time course, CCL2 and CCR2 were expressed in astroglia and granulocytes only on level T9; there was additional astroglial CCL2 expression in dorsal columns and dorsal horns above and below T9 of severely injured animals 42d after lesion. In dorsal horns (level L3-L5) of animals exhibiting chronic below-level pain CCL2 was co-expressed with transmitters and receptors that are involved in nociceptive processing like calcitonin gene-related peptide (CGRP), Substance-P, vanilloid-receptor-1, and its activated phosphorylated form. These data demonstrate lesion grade dependence of below-level pain development and suggest chemokines as potential candidates for integrating inflammation and central neuropathic pain after SCI.
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PMID:Force-dependent development of neuropathic central pain and time-related CCL2/CCR2 expression after graded spinal cord contusion injuries of the rat. 1833 59

The underlying mechanism for electroacupuncture (EA) associated functional improvement in patients suffering from spinal cord injury (SCI) is largely unknown. Collateral sprouting is one plausible factor, where the cord microenvironment may contribute greatly. The present study evaluated the effects of EA on collateral sprouting from spared dorsal root ganglion (DRG), sensory functional restorations, and differential gene expressions in spinal cord after partial DRG removal in the rat. Following EA, N1 waveform latencies for cortical somatosensory evoked potential significantly shortened. The densities of terminal sprouting from the spared DRG significantly increased on the EA versus the non-EA side. Microarray analysis revealed that several genes were upregulated on the acupunctured side at different time points; they were ciliary neurotrophic factor (CNTF) at 1 day postoperation (dpo), fibroblast growth factor (FGF)-1, insulin-like growth factor (IGF) 1 receptor, neuropeptide Y, and FGF-13 at 7 dpo, and CNTF and calcitonin gene-related polypeptide-alpha at 14 dpo, respectively. Meanwhile, five genes (CNTF, p75-like apoptosis-inducing death domain protein, IGF-1, transforming growth factor-beta 2, and FGF-4) were downregulated at 7 dpo. Furthermore, reverse transcriptase polymerase chain reaction results supported the gene chip analysis. It was concluded that the EA induced sensory functional restorations following partial DRG ganglionectomies could be brought about by intraspinal sprouting from the spared DRG, as well as multiple differential gene expressions in the spinal cord. The results could have clinical application in EA treatment of patients after spinal injury.
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PMID:Electroacupuncture induced spinal plasticity is linked to multiple gene expressions in dorsal root deafferented rats. 1858 Dec 69

In a retrospective case series study, medical records were evaluated for all male patients infected with human immunodeficiency virus (HIV) diagnosed over a one-year period with foot fractures (n = 30) confirmed by magnetic resonance imaging at a Los Angeles outpatient private practice rheumatology clinic. Proportionally more patients had received tenofovir prefracture (17 [57%]) than those who had not (13 [43%]). At fracture diagnosis, these two groups were similar in median age (49 versus 48 years), HIV-1 RNA (both 1.7 log(10) copies/mL), CD4 count (300 versus 364/mm(3)), time between HIV diagnosis and foot fracture (both 17 years), family history of degenerative bone disease (24% versus 23%), prevalence of malabsorption syndrome, renal failure, calcium deficiency, or vitamin D deficiency, and concurrent use of bisphosphonates, calcitonin, and diuretics. However, more tenofovir-treated patients had osteoporosis (35% versus 8%), stress-type fractures (53% versus 31%), concurrent fractures (12% versus 0%), wasting syndrome (29% versus 15%), truncal obesity (18% versus 8%), smoked cigarettes (more than one pack/day for more than one year; 35% versus 8%), dual energy X-ray absorptiometry (DEXA) T scores < -2.4 (denoting osteoporosis) at the femur (24% versus 9%) and spine (47% versus 36%), and had received protease inhibitors (71% versus 46%), non-nucleoside reverse transcriptase inhibitors (24% versus 0%), prednisone (24% versus 0%), testosterone (47% versus 23%), and teriparatide (29% versus 8%). Median time from tenofovir initiation until fracture was 2.57 (range 1.17-5.69) years. In conclusion, more foot fractures were observed in tenofovir-treated patients than in non-tenofovir-treated patients with HIV infection. Comorbidities and/or coadministered drugs may have been contributory.
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PMID:Characteristics of foot fractures in HIV-infected patients previously treated with tenofovir versus non-tenofovir-containing highly active antiretroviral therapy. 2209 7

Previous studies showed that 5-hydroxytryptamine (5-HT)(1B/1D) receptor stimulation by triptans alleviates neuropathic pain caused by chronic constriction injury to the infraorbital nerve (CCI-ION) but not the sciatic nerve (CCI-SN) in rats. To assess whether such differential effects in the cephalic vs extracephalic territories is a property shared by other antimigraine drugs, we used the same models to investigate the effects of olcegepant, which has an antimigraine action mediated through calcitonin gene-related peptide (CGRP) receptor blockade. Adult male rats underwent unilateral CCI to the ION or the SN, and subsequent allodynia and/or hyperalgesia were assessed in ipsilateral vibrissal territory or hindpaw, respectively, using von Frey filaments and validated nociceptive tests. c-Fos expression was quantified by immunohistochemistry and interleukin 6 and activating transcription factor 3 (ATF3) mRNAs by real-time quantitative reverse transcriptase-polymerase chain reaction. Like naratriptan (0.1 to 0.3mg/kg, subcutaneously), olcegepant (0.3 to 0.9mg/kg, intravenously) markedly reduced mechanical allodynia in CCI-ION rats. In contrast, in CCI-SN rats, mechanical allodynia was completely unaffected and hyperalgesia was only marginally reduced by these drugs. A supra-additive antiallodynic effect was observed in CCI-ION rats treated with olcegepant (0.3mg/kg intravenously) plus naratriptan (0.1mg/kg subcutaneously), whereas this drug combination remained inactive in CCI-SN rats. Olcegepant (0.6mg/kg, intravenously) significantly reduced the number of c-Fos immunolabeled cells in spinal nucleus of the trigeminal nerve and upregulation of ATF3 transcript (a marker of neuron injury) but not that of interleukin-6 in trigeminal ganglion of CCI-ION rats. These findings suggest that CGRP receptor blockade might be of potential interest to alleviate trigeminal neuropathic pain.
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PMID:Differential effects of calcitonin gene-related peptide receptor blockade by olcegepant on mechanical allodynia induced by ligation of the infraorbital nerve vs the sciatic nerve in the rat. 2279 18


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