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)

The aim in this study was to investigate if our new experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could reduce overexpression of inflammatory mediators during reperfusion. Stroke in Sprague-Dawley rats (n=24) was induced by a 2-h middle cerebral artery occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 12 of the ischemic rats received 6 ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Expression of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule 1 (ICAM-1) mRNA was analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant overexpression (9-26 fold) of the genes encoding TNF-alpha, IL-1beta and ICAM-1 in ischemic rats was found during early reperfusion without flushing at 6 and 12 h. This increase was significantly reduced at both 6 and 12 h post-reperfusion as a result of saline flushing.
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PMID:Reduced inflammatory mediator expression by pre-reperfusion infusion into ischemic territory in rats: a real-time polymerase chain reaction analysis. 1466 9

The aim in this study was to investigate whether our experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could ameliorate disruption of microvascular integrity by reducing matrix metalloproteinase (MMP) expression during reperfusion. Stroke in Sprague Dawley rats (n = 42) was induced by a 2-h right middle cerebral artery (MCA) occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 24 of the ischemic rats received 6ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Brain edema was determined by comparing the percentage difference in brain volume between the right and left (contralateral to stroke site) hemispheres, while the expressions of MMP-2 and -9 mRNA were analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant (p < 0.01) brain edema, determined by an increased brain volume of 19 +/- 4%, and overexpression of the mRNA encoding MMPs, determined by increased relative mRNA level ratio, were found in ischemic rats. The brain damage, in terms of brain edema (4 +/- 1%) and overexpression of MMPs, was significantly (p < 0.05) ameliorated as a result of saline flushing into the ischemic territory prior to reperfusion. This study has enhanced our understanding of the causal mechanisms by which the neuroprotective effect of ischemic area "flushing" can be achieved.
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PMID:Reduced brain edema and matrix metalloproteinase (MMP) expression by pre-reperfusion infusion into ischemic territory in rat. 1553 Oct 84

There is evidence that physical activity is associated with decreased brain injury resulting from transient middle cerebral artery (MCA) occlusion. We investigated whether exercise could reduce stroke-induced brain inflammatory injury and its associated mediators. Sprague Dawley rats (3 months old) were subjected to 30 min exercise on a treadmill each day for 1-3 weeks. Stroke, in exercised and non-exercised animals, was then induced by a 2-h MCA occlusion followed by 48 h of reperfusion using an intraluminal filament. Endothelial expression of the intercellular adhesion molecule 1 (ICAM-1) and leukocyte infiltration were determined by immunocytochemistry. Expressions of tumor necrosis factor-alpha (TNF-alpha) and ICAM-1 mRNA were detected using a real-time reverse transcriptase-polymerase chain reaction in ischemic rats with or without exercise, and in non-ischemic control rats following exercise. Expression of TNF-alpha increased after exercise for 2 and 3 weeks. The overexpression of TNF-alpha was not further elevated in 3-week exercised rats subjected to a transient MCA occlusion and 6 or 12 h of reperfusion, as compared to that in non-exercised rats. Furthermore, ICAM-1 mRNA expression remained at significantly (P<0.01) low levels in exercised animals during ischemia/reperfusion. Pre-ischemic exercise significantly (P<0.01) reduced numbers of ICAM-1-positive vessels and infiltrating leukocytes in the frontoparietal cortex and dorsolateral striatum in ischemic rats after 48 h of reperfusion. Exercised ischemic rats demonstrated an 11+/-7% infarct volume of contralateral hemisphere as compared to a 52+/-3% volume in non-exercised ischemic rats. The data suggests that exercise inhibits inflammatory injury (i.e., decreased expression of inflammatory mediators and reduced accumulation of leukocytes) during reperfusion, leading to reduced brain damage. Chronically increased expression of TNF-alpha during exercise prevent the same downstream inflammatory events as does acutely elevated TNF-alpha after ischemia/reperfusion.
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PMID:Exercise preconditioning ameliorates inflammatory injury in ischemic rats during reperfusion. 1561 90

Hypericin is a naturally occurring substance found in the common St. John's Wort (Hypericum species) and can also be synthesized from the anthraquinone derivative emodin. As the main component of Hypericum perforatum, it has traditionally been used throughout the history of folk medicine. In the last three decades, hypericin has also become the subject of intensive biochemical research and is proving to be a multifunctional agent in drug and medicinal applications. Recent studies report antidepressive, antineoplastic, antitumor and antiviral (human immunodeficiency and hepatitis C virus) activities of hypericin; intriguing information even if confirmation of data is incomplete and mechanisms of these activities still remain largely unexplained. In other contemporary studies, screening hypericin for inhibitory effects on various pharmaceutically important enzymes such as MAO (monoaminoxidase), PKC (protein kinase C), dopamine-beta-hydroxylase, reverse transcriptase, telomerase and CYP (cytochrome P450), has yielded results supporting therapeutic potential. Research of hypericin and its effect on GABA-activated (gamma amino butyric acid) currents and NMDA (N-methyl-D-aspartat) receptors also indicate the therapeutic potential of this substance whereby new insights in stroke research (apoplexy) are expected. Also in the relatively newly established fields of medical photochemistry and photobiology, intensive research reveals hypericin to be a promising novel therapeutic and diagnostic agent in treatment and detection of cancer (photodynamic activation of free radical production). Hypericin is not new to the research community, but it is achieving a new and promising status as an effective agent in medical diagnostic and therapeutic applications. New, although controversial data, over the recent years dictate further research, re-evaluation and discussion of this substance. Our up-to-date summary of hypericin, its activities and potentials, is aimed to contribute to this process.
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PMID:Hypericin--the facts about a controversial agent. 1563 60

Several studies have suggested that adult haematopoietic stem cells (HSCs) may be capable of transdifferentiating across tissue-lineage boundaries, giving rise to the concept that these stem cells are plastic in their differentiative capacity. This topic created much excitement in the scientific community, with the prospect of employing HSCs in tissue/organ regeneration (e.g. heart infarct, stroke, liver damage) as an alternative to multipotent embryonic stem cells. However, recent observations, and several alternative explanations of previously published data (e.g. cell fusion, epigenetic changes), do not support the concept of HSC plasticity. Our recent studies, in which we employed chemotactic isolation to a stromal-cell-derived-factor-1 (SDF-1) gradient combined with real-time reverse transcriptase (RT)-PCR/immuno-histochemical analyses, revealed that bone marrow (BM) contains a highly mobile population of CXCR4+ cells that express mRNA/proteins for various markers of early tissue-committed stem cells (TCSCs). Based on this we postulate that the BM is not only a home for HSCs, but also a 'hideout' for non-haematopoietic CXCR4+ TCSCs, and we suggest that their presence in BM tissue should be considered before experimental evidence is interpreted simply as transdifferentiation/plasticity of HSCs. Furthermore, our observation that the number of TCSCs is the highest in BM of young animals and decreases with age provides a novel insight into aging, and may explain why the regeneration process becomes less effective in older individuals.
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PMID:Bone marrow as a source of circulating CXCR4+ tissue-committed stem cells. 1565 79

The purpose of this study was to determine if exercise could induce expression of vascular endothelial growth factor (VEGF) and angiopoietin 1 and 2, in association with angiogenesis; and if angiogenic changes correlated with reduced brain injury in stroke. Adult male Sprague Dawley rats (3 month old, n=44) were exercised on a treadmill 30 minutes each day for 1, 3 or 6 weeks, or housed as non-exercised controls for 3 weeks. Some 3 week-exercised rats were then housed for an additional 3 weeks. Exercise significantly (p<0.01) increased mRNA (determined by real-time reverse transcriptase-polymerase chain reaction) expression of angiopoietin 1 and 2 as early as 1 week, with further increases occurring at 3 weeks. A mild increase after 1 week and a robust increase after 3 weeks of exercise in four isoforms (120, 144, 164, 188) of VEGF mRNA levels were significantly (p<0.01) observed, with VEGF(144) being more markedly up-regulated. Overexpression of the mRNAs decreased upon withdrawal of exercise. A significant increase (p<0.01) in the density of microvessels (determined by laminin-immunocytochemistry) was found at 3 weeks of exercise and this continued after exercise was withdrawn. In exercising rats subjected to 2-h MCA occlusion followed by 48-h reperfusion, neurological deficits and infarct volume were significantly reduced. Neuroprotection continued after 3 weeks of rest. This study indicates that pre-ischemic exercise reduces brain injury in stroke. The reduced damage is associated with angiogenesis, possibly induced by angiogenic factors following exercise. Physical exercise up-regulates mRNA levels of the angiopoietin family and VEGF.
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PMID:Exercise-induced overexpression of angiogenic factors and reduction of ischemia/reperfusion injury in stroke. 1618 Oct 89

Activins are members of the transforming growth factor-beta superfamily that exert neurotrophic and neuroprotective effects on various neuronal populations. To determine the possible function of activin in stroke injury, we assessed which components of the activin signalling pathway were modulated in response to middle cerebral artery occlusion (MCAO). Furthermore, because oestradiol replacement protects against MCAO-induced cell death, we explored whether oestradiol replacement influences activin gene expression. Female Sprague-Dawley rats underwent permanent MCAO and the expression of activins and their corresponding receptors was determined by semiquantitative reverse transcriptase-polymerase chain reaction at 24 h after onset of ischaemia. We observed up-regulation of activin betaA and activin type I receptor A mRNA in response to injury. Dual-label immunocytochemistry followed by confocal z-stack analysis showed that the activin A expressing cells comprised neurones. Next, we monitored the time course of activin betaA mRNA expression in oestradiol- or vehicle-treated rats at 4, 8, 16 and 24 h after MCAO via in situ hybridisation. Starting at 4 h after injury, activin betaA mRNA was up-regulated in cortical and striatal areas in the ipsilateral hemisphere. Activin betaA mRNA levels in the cortex increased dramatically with time and were highest at 24 h after the insult, and oestradiol replacement did not influence this increase.
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PMID:Stroke injury in rats causes an increase in activin A gene expression which is unaffected by oestradiol treatment. 1642 Feb 78

Increased expression of tumor necrosis factor alpha (TNFalpha) has been shown in adult stroke models. However, its expression and relationship with neuronal apoptosis in neonatal rats with transient middle cerebral artery occlusion (MCAO) have not been clearly elucidated. We studied the expression and distribution of TNFalpha and neuronal apoptosis in a postnatal Day 10 rat MCAO model using reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot, immunohistochemistry, fluorescence double-labeling, and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) analyses. We found TNFalpha mRNA expression increased at 2h and was maintained at high levels until 24h after reperfusion. TNFalpha protein expression was significantly increased from 4 to 8h (p < 0.01) lasting through 24h (p < 0.05) after reperfusion compared to the sham controls. TNFalpha immunoreactive cells were colocalized to neurons in both the core and the penumbra areas of the ischemic cortex. However, apoptotic cells were mainly distributed in the penumbra area and colocalized to neurons as well as to TNFalpha immunoreactive cells in the ischemic cortex. Our findings suggest that TNFalpha expression increases after neonatal stroke and is associated with neuronal apoptosis after transient focal cerebral ischemia.
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PMID:Expression of tumor necrosis factor alpha and neuronal apoptosis in the developing rat brain after neonatal stroke. 1679 40

Neural progenitor cells in the subventricular zone (SVZ) of the lateral ventricular wall give rise to new neurons throughout rodent life. Ischemic stroke induces angiogenesis and neurogenesis. Using laser capture microdissection (LCM) in combination with microarrays containing approximately 400 known genes associated with stem cells and angiogenesis, we investigated gene profiles of SVZ cells in the adult mouse subjected to middle cerebral artery occlusion. Our data revealed that nonstroke SVZ cells expressed sets of genes that are important for neural progenitor cell proliferation, differentiation, and migration. In addition, stroke SVZ cells expressed many genes involved in neurogenesis during embryonic development but were not detected in nonstroke SVZ cells. Stroke upregulated genes were verified by real-time reverse transcriptase-polymerase chain reaction and immunostaining. These data indicate that adult SVZ cells recapture embryonic molecular signals after stroke and provide insight into the molecular mechanisms, which regulate the biological function of neural progenitor cells in the SVZ of adult rodent brain under physiological and stroke conditions.
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PMID:Stroke induces gene profile changes associated with neurogenesis and angiogenesis in adult subventricular zone progenitor cells. 1683 28

Exercise reduces ischemia and reperfusion injury in rat stroke models. We investigated whether gradual increases in tumor necrosis factor-alpha (TNF-alpha) reported during exercise down-regulates expression of TNF-alpha receptors I and II (TNFRI and II) in stroke, leading to reduced brain damage. Adult male Sprague Dawley rats were subjected to 30 minutes of exercise on a treadmill each day for 3 weeks. Then, stroke was induced by a 2-hour middle cerebral artery (MCA) occlusion using an intra-luminal filament. Expressions of TNFRI and II mRNA in the brain were detected using a real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Protein expressions of TNFRI and II were determined by enzyme-linked immunoabsorbant assay (ELISA) in serum and brain homogenates. Spatial distribution of TNF-alpha receptors in brain regions was determined with immunocytochemistry. In human umbilical vein endothelial cells (HUVEC), we addressed the causal effect of TNF-alpha pretreatment on TNF I and II expression using ELISA and real-time PCR. In exercised rats after stroke, brain infarct was significantly (p<0.01) reduced in the entire MCA supplied regions, associated with a mild expression of TNFRI and II mRNA and protein. The TNF-alpha receptors were restricted to the ischemic core. In contrast, a robust expression of TNFRI and II molecules was found in non-exercised rats subjected to similar ischemia/reperfusion insults. An in vitro study revealed a causal link between TNF-alpha pretreatment and reduced cellular expression of TNF-alpha receptors under hypoxic/reoxygenated conditions. Our results suggest that reduced-brain damage in ischemic rats after exercise preconditioning may be attributable to the reduced expression of TNF-alpha receptors. Chronically increased TNF-alpha expression was also found to reduce TNFI and II responding to acute ischemia/reperfusion insult.
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PMID:Exercise preconditioning reduces brain damage and inhibits TNF-alpha receptor expression after hypoxia/reoxygenation: an in vivo and in vitro study. 1710 21


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