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)

While the role of cytokines in mediating injury during hind limb skeletal muscle ischemia followed by reperfusion has recently been described, the role of cytokines in myocardial infarction and ischemia/reperfusion have remained relatively unexplored. We hypothesize that cytokines play an important role in the regulation of postischemic myocardial inflammation. This study reports the temporal sequence of proinflammatory cytokine gene expression in postischemic/reperfused myocardium and localizes interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha)-protein by immunostaining. Rats were subjected to either permanent left anterior descending (LAD) occlusion or to 35 minutes of LAD occlusion followed by reperfusion and sacrificed up to 7 days later. Rat-specific oligonucleotide probes were used to semiquantitatively assess the relative expression of mRNA for TNF-alpha, IL-1 beta, IL-2, IL-6, interferon-gamma (IFN-gamma), and transforming growth factor-beta 1 (TGF-beta 1) utilizing the reverse transcriptase-polymerase chain reaction amplification technique. Increased cardiac mRNA levels for all cytokines except IL-6 and IFN-gamma were measurable within 15 to 30 minutes of LAD occlusion and increased levels were generally sustained for 3 hours. During early reperfusion, mRNA levels for IL-6 and TGF-beta 1 were significantly reduced compared with permanent LAD occlusion. In both groups, cytokine mRNA levels all returned to baseline levels at 24 hours, while IL-1 beta, TNF-alpha, and TGF-beta 1 mRNA levels again rose significantly at 7 days only in animals with permanent LAD occlusion. Immunostaining for IL-1 beta and TNF-alpha protein revealed two patterns of reactivity: 1) microvascular staining for both IL-1 beta and TNF-alpha protein only in postischemic reperfused myocardium in early post-reperfusion time points; and 2) staining of infiltrating macrophages in healing infarct zones which was most prominent at 7 days after permanent LAD occlusion. These results provide evidence for local expression of cytokine mRNA in postischemic myocardium and suggest that regulation of local cytokine release is altered during the postischemic period.
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PMID:Cytokine mRNA expression in postischemic/reperfused myocardium. 785 52

The myocardial ischemia and reperfusion injury is caused by the re-introduction of coronary circulation in ischemic myocardial tissues. A number of experiments demonstrate that immunological response such as adherence of neutrophils to endothelial cells play a critical role in reperfusion injury. In this paper, the effect of global ischemia and reperfusion on the expression of cytokine genes by myocardial tissues as well as cell adhesion molecules by neutrophils were studied by using Langendorff model. Cardiac dysfunction and immunological response in 25 min global ischemia at 37.5 degrees C followed by 60 min reperfusion were studied in isolated rat heart perfused with blood supplied from support rat (Langendorff model). Cardiac functions were measured with a left intraventricular balloon. The mean post-experimental reduction of the left ventricular end-systolic pressure were 87.5 +/- 1.6% of pre-experimental level in the control perfusion group and 55.5 +/- 5.8% in the reperfusion group. Immunofluorescence flow cytometry showed that ischemia and reperfusion injury did not affect the expression of adhesion molecules on neutrophils which were isolated from perfused blood samples. Cytokine gene expression was analyzed by direct analysis of mRNA obtained from the blood-perfused, isolated rat heart. The level of expression of the cytokine genes was assessed using semiquantitative reverse transcriptase-polymerase chain reaction (semiquantitative RT-PCR). IL-6, IL-8, IFN-gamma, TNF-alpha were expressed in normal heart tissue at low level and were upregulated following ischemia and reperfusion. IL-1 beta, MCP-1 and IL-1 receptor antagonist were not expressed at detectable level in normal heart but were induced following global ischemia. IL-1 alpha was not expressed at detectable level in normal heart but was induced following reperfusion of the ischemic heart. Histological examination of myocardial tissue from the reperfusion group revealed no evidence of myocardial necrosis. Only a mild interstitial edema as well as weak focal hemorrhage was detected after reperfusion of ischemic hearts. These results suggest that there is a process which causes early stage of post-ischemic myocardial dysfunction without involving myocardial necrosis nor infiltration of inflammatory cells.
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PMID:[Cardiac dysfunction and endogenous cytokines in global ischemia and reperfusion injury]. 811 7

A reverse transcriptase-polymerase chain reaction (RT-PCR) product obtained from ischemic rat brain RNA was used to screen a rat ischemic forebrain cDNA library for a cDNA clone containing the entire open reading frame for the inducible hsp70. The coding sequence for the rat hsp70 cDNA demonstrated significant similarities with the human hsp70 of Hunt and Morimoto (Proc Natl Acad Sci 82:6455-6459, 1985) and the mouse hsp70 of Hunt and Calderwood (Gene 87:199-204, 1990). The rat inducible hsp70 and constitutive hsc73 sequences are distinct. There was a low level of hsp70 mRNA expression in normal rat brain as in found in other tissues. hsp70 mRNA was markedly induced in rat brain 8 hours following global ischemia and kainic acid-induced seizures. Northern blots showed a approximately 2.9kb hsp70 mRNA band from control, kainic acid, and ischemic brains. RT-PCR confirmed the presence of hsp70 mRNA in normal rat brain. Since there are at least five human and six mouse inducible hsp70 genes known, many other rat hsp70 genes probably exist that could function in different cells or organelles or be induced under different circumstances.
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PMID:cDNA cloning and expression of stress-inducible rat hsp70 in normal and injured rat brain. 827 11

Expression and function of the beta 2-adrenergic receptor (beta 2-AR), a critical modulator of motor function, is altered in ischemic tissues. However, the mechanism by which ischemia influences gene expression remains controversial, in part because of the conflicting results reported by numerous investigators. To determine the relative importance of hypoxia and acidosis on beta 2-AR expression and function, steady-state mRNA levels and receptor function were measured in DDT1MF-2 hamster smooth muscle cells grown in 10% serum and 3 nM epinephrine in 5% CO2 (pH 7.50) and then exposed for 48 h to either combined hypoxia with acidosis (through incubation in 2% O2, 10% CO2, mean pH 7.14 at 48 h), hypoxia alone (2% O2, 2.5% CO2, pH 7.36), normoxia-acidosis (21% O2, 10% CO2, pH 7.12) or continued normoxia (21% O2, 2.5% CO2, pH 7.49). Combined hypoxia-acidosis downregulated the beta 2-AR membrane density by 50% compared to hypoxia alone and normoxia alone at 48 h. beta 2-AR coupling in these cells, as measured by cellular cAMP production in response to 10(-4) M isoproterenol, was decreased by hypoxia but increased by acidosis. The effect of hypoxia-acidosis on Bmax was abolished by inhibiting transcription with 1.0 microgram/ml actinomycin D. A quantitative reverse transcriptase polymerase chain reaction assay demonstrated a decrease in steady-state mRNA concentration with hypoxia-acidosis. Our experiments demonstrate an important distinction between the effects of modeled hypoxia and ischemia on beta 2-AR gene expression.
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PMID:pH is critical to the regulation of expression of the beta 2-adrenergic receptor gene in hypoxia. 897 14

Granulocyte colony-stimulating factor (G-CSF) is the cytokine that is critical for polymorphonuclear neutrophilic granulocyte (PMN) production as well as being a potent agonist of PMN activation. We have recently reported that in the lung and the liver of rats resuscitated after hemorrhagic shock (HS) G-CSF mRNA expression is induced. It is not known if both phases of HS, the ischemic and the reperfusion phase, are required for G-CSF mRNA induction. The present study was designed to test the hypothesis that the upregulation of G-CSF mRNA expression is the consequence of HS followed by resuscitation and that ischemia alone is insufficient to induce G-CSF mRNA expression in the affected organs. Male Sprague-Dawley rats were subjected to resuscitated and unresuscitated shock protocols of varying severity. Control animals were subjected to anesthesia and all surgical preparations except for hemorrhage. Lungs and livers were isolated and their RNA extracted. Using semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we demonstrated that G-CSF mRNA was induced in the lung and liver of shock animals above the level observed in control animals. Upregulation of G-CSF mRNA relative to controls occurred only in animals undergoing resuscitated HS and not in ones subjected to unresuscitated HS. These results indicate that G-CSF production specific for the hemorrhage component of shock is dependent on resuscitation. As a consequence, the production of this cytokine may be decreased through modifications in the resuscitation protocols.
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PMID:Granulocyte colony-stimulating factor (G-CSF) production in hemorrhagic shock requires both the ischemic and resuscitation phase. 906 Nov 73

Phospholipase A2 has been considered to play a role in physiological membrane turnover in cardiac tissue and in the degradation of membrane lipids under pathophysiological conditions, such as ischemia and reperfusion. We report the cloning of a cDNA encoding a member of the Ca2+-dependent, low molecular mass phospholipase A2 (PLA2) present in rat heart. The cDNA predicts a mature protein of 146 amino acid residues including a 21 amino acid sequence at the N-terminal end, which has the features characteristic of eukaryotic secretory signal peptides. The deduced amino acid sequence constitutes an enzyme of the group II class of PLA2s, and resembles PLA2s from other mammalian sources. A Northern blot analysis performed to determine the tissue distribution showed that rat ileum contains the largest amount of the PLA2 transcript among the tissues examined, a weaker signal was present in heart, spleen and soleus muscle, and no signal could be detected in EDL muscle, stomach, liver, kidney, brain and lung. Northern blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR) techniques indicate the presence of this enzyme in neonatal and adult rat cardiomyocytes and in a cultured rat cardiac fibroblast-like cell line, but not in rat cardiac-derived endothelial cell lines. Transcription levels of rat heart group II PLA2 in isolated neonatal rat cardiomyocytes were found to increase after stimulating the cells with tumor necrosis factor-alpha (TNF-alpha) or the alpha1-adrenergic agonist phenylephrine.
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PMID:Cloning and cellular distribution of a group II phospholipase A2 expressed in the heart. 928 42

Transient global or focal ischemia leads to the production of several types of lesions in the DNA backbone including alkali-labile sites, and both single-stranded (ss) and double-stranded (ds) breaks. The ds breaks result in high molecular weight fragments of 10-50 kbp that contain both 3'- and 5'-OH end-groups, suggesting that more than one endonuclease is involved. This lesioning of DNA is followed by the appearance of the damage-response indicator Gadd45 in the ischemic hemisphere following middle cerebral artery occlusion. By 6 h, gadd45 mRNA was shown to increase by semi-quantitative reverse transcriptase - polymerase chain reaction. In situ hybridization histochemistry indicated that these increases in gadd45 mRNA occurred in pyramidal neurons located on the edge of the infarcted cortex. Gadd45 immunostaining yielded similar findings with maximal protein staining detected at 18 h after occlusion. In neurons, in the infarct core with frank DNA fragmentation shown by in situ TdT-mediated dUTP-biotin nick end labeling (TUNEL) at 24 h, the Gadd45 immunostaining was not visible. Taken together, these findings suggest that Gadd45 responds to DNA damage following ischemia as part of a repair response mounted by brain cells attempting to survive the insult.
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PMID:Increases in DNA lesions and the DNA damage indicator Gadd45 following transient cerebral ischemia. 949 61

In experimental models, the synthesis of heat shock protein 70 (HSP 70) has been recognized as an intracellular response to ischemia and reperfusion, insults inherent to transplantation. In this study, the HSP response in early stages of human liver transplantation was investigated. HSP 70 mRNA expression was detected by means of reverse transcriptase (RT)-PCR in liver biopsies (n = 28) and in cells obtained from the organ perfusate (n = 14) following cold preservation. The expression of HSP 70 differed substantially between individuals. Retrospective analysis revealed a close correlation of the amount of HSP 70 mRNA in perfusate cells and biopsies with the onset of organ dysfunction due to early graft rejection. Patients with early graft rejection had a significantly lower amount of HSP 70 mRNA than patients without rejection. These results suggest a protective role of HSP 70 expression. Low levels of HSP 70 may, therefore, represent a prognostic marker for early graft rejection.
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PMID:Expression of HSP 70 as a potential prognostic marker for acute rejection in human liver transplantation. 956 74

Chemokine receptors play a crucial role in the recruitment of immune cells to sites of inflammation. Although chronic diseases of the brain are often accompanied by inflammatory events, there is presently no information about the occurrence and regulation of these receptors in the central nervous system (CNS). Moreover, one CC-chemokine receptor, CKR5, has recently been identified as coreceptor for HIV-1 entry into macrophages. HIV-1 target cells in brain are macrophage-related microglia, which suggests that they are infected by the same mechanism (He et al.,: Nature 385:645-649, 1997). Although rats are not susceptible to HIV-1 infection, they can be used to study chemokine receptor regulation in a variety of brain pathologies. After cloning CC-CKR5 and establishing reverse transcriptase polymerase chain reaction (RT-PCR) for its ligands macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and regulated on activation, normal T cell-expressed and secreted (RANTES), we studied expression of these four mRNAs in purified microglia and compared it with their expression in rat brain. Lipopolysaccharide (LPS)-treated microglia showed transiently increased mRNA levels of both CKR5 and its ligands. Similar data were obtained from brains of LPS-injected rats. In middle cerebral artery occluded (MCAO)-animals, RANTES mRNA was unaffected, whereas CKR5 mRNA showed a sustained rise until 96 hr after surgery. MIPs exogenously added to microglial cultures markedly reduced CKR5 mRNA expression, whereas RANTES did not. MIP mRNAs, in contrast to RANTES and CKR5 mRNAs, were undetectable in normal brain. RANTES appears to play a role distinct from MIPs in brain. In summary, upregulation of CC-chemokines and CKR5 in the CNS upon bacterial infection or in ischemia may impact on microglial activation stage and result in increased risk of HIV-1 infection.
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PMID:Cloning of rat HIV-1-chemokine coreceptor CKR5 from microglia and upregulation of its mRNA in ischemic and endotoxinemic rat brain. 967 Sep 89

Our previous studies showed that the amount of endogenous basic fibroblast growth factor (bFGF) was reduced after ischemia and reperfusion insult. One of the mechanisms involved in the decrease of endogenous bFGF is the increased destruction of this growth factor associated with oxygen free radical activation and inflammation. We hypothesized that the wounding also impairs the secretion of bFGF and examined the bFGF gene expression in skeletal muscles after ischemia and reperfusion insult. In this study, a rat leg ischemia (4 h) and reperfusion (24 h) injury model was prepared and the in situ hybridization method and reverse transcriptase polymerase chain reaction technique (RT-PCR) were used to evaluate the bFGF gene expression and its localization in control (normal) and injured rat skeletal muscles. The results showed that the bFGF mRNA expression was localized in the cytoplasm in control skeletal muscle, especially at the periphery inside the cells. According to the intensity of the stain, four main classes of fibers could be identified: strongly, moderately, weakly, and negatively stained fibers. Based on the positive stain, about 82% of the total fibers examined were positive for bFGF mRNA stain. In ischemic or ischemic and reperfused rat skeletal muscles, the localization of bFGF mRNA expression was similar to that in normal skeletal muscles, but only 52% in ischemic muscles and 22% in ischemic and reperfused muscles had positive bFGF mRNA staining. RT-PCR confirmed a significant decrease in bFGF mRNA expression in ischemic and reperfused rat skeletal muscles. These results suggest that the acute ischemia and reperfusion not only induce the destruction of endogenous bFGF molecule, which is stored at the extracellular matrix of the fibers, but also downregulate the bFGF gene expression. The simultaneous dysregulation of endogenous bFGF gene expression and decreased synthesis of bFGF protein suggest a possible role of this growth factor in delayed wound healing.
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PMID:Ischemia and reperfusion impair the gene expression of endogenous basic fibroblast growth factor (bFGF) in rat skeletal muscles. 979 Aug 20


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