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actinomycin d/hypoxia
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Pagina 1 a partire dal 133 risultati
Plasma aldosterone concentration during hypoxia, stimulated hyperglycaemia and when protein synthesis is blocked with actinomycin D.
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In order to study the effect of various agents on aldosterone secretion, the aldosterone concentration was determined radioimmunologically in 41 rats divided in groups: group I--7 rats--controls; group II--11 rats loaded p.o. with 5.5% glucose solution in doses of 2.4 ml/100 g body weight, taking
[Effect of actinomycin-D on erythropoietin synthesis during hypoxia in the rat].
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Both increased stability and transcription contribute to the induction of the urokinase plasminogen activator receptor (uPAR) message by hypoxia.
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Both hypoxia and overexpression of the urokinase plasminogen activator receptor (uPAR) are associated with a poor clinical outcome in human cancers. Hypoxia has been shown to induce uPAR expression in breast cancer cells and to increase their invasion through Matrigel, a phenomenon which can be
Hypoxia decreases constitutive nitric oxide synthase transcript and protein in cultured endothelial cells.
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Endothelial cell-generated nitric oxide (NO) accounts in large part for the labile vasodilator termed endothelium-derived relaxing factor. Two distinct types of NO synthase exist: a "constitutive' type (cNOS), found in endothelial cells, and an "inducible' enzyme. Endothelial cells sense pO2 levels
A comparison of non-viral vectors for gene delivery to pancreatic beta-cells: delivering a hypoxia-inducible vascular endothelial growth factor gene to rat islets.
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Although non-viral vectors are relatively safe, they have very low gene transfection efficiency, especially in pancreatic islet cells. To provide information on the use of non-viral vectors for transfecting genes into pancreatic islet cells, a comparative evaluation of non-viral options was
Hypoxia downregulates tropoelastin gene expression in rat lung fibroblasts by pretranslational mechanisms.
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Elastolytic lung injury disrupts cell barriers, flooding alveoli and producing regional hypoxia. Abnormal O2 tensions may alter repair of damaged elastin fibers. To determine the effect of hypoxia on extravascular elastin formation, we isolated rat lung fibroblasts and cultured them under a variety
[Effect of bemethyl on the glutathione system in the rat liver in acute hypoxia].
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The effect of bemithyl on the state of liver glutathione system was studied in rats under acute hypoxic hypoxia conditions modeled by "elevating" animals in a pressure chamber up to an altitude of 8000-11,000 m for 30 min. Bemithyl (25 mg/kg, i.p.) administered 30 min before the hypoxia onset,
Evidence for hypoxia-induced, programmed cell death of cultured neurons.
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Apoptosis, a form of cell death ("programmed" cell death) in which the nucleus and cytoplasm shrink and often fragment, serves to eliminate excessive or unwanted cells during remodeling of embryonic tissues, during organ involution, and in tumor regression. In acute pathological states, such as
Hypoxia-specific upregulation of calpain activity and gene expression in pulmonary artery endothelial cells.
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The effects of exposure to hypoxia on the catalytic activity and mRNA expression of calpain, a calcium-regulated neutral cysteine protease, were examined in porcine pulmonary artery endothelial cells (PAECs). Specificity of the response to hypoxia was determined by comparing the effects of hypoxic
Modulation of inducible nitric oxide synthase by hypoxia in pulmonary artery endothelial cells.
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The effects of hypoxia on the regulation of inducible nitric oxide synthase (NOS) 2 expression were examined in cultured rat pulmonary microvascular endothelial cells (EC). EC did not express NOS 2 mRNA or protein when exposed to normoxia or hypoxia unless they were pretreated with interleukin
Hypoxemia regulates effect of lipopolysaccharide on polymorphonuclear leukocyte CD11b/CD18 expression.
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Expression of the receptor CD11b/CD18 on the polymorphonuclear leukocyte (PMN) surface is important for several aspects of PMN function during endotoxemia. The mechanisms underlying regulation of CD11b/CD18 expression during hypoxemia and endotoxemia, however, are less clear. We investigated the
[Protective effect of BAG-1L mediated by lentivirus in human neuroblastoma cells induced by hypoxia].
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OBJECTIVE
To investigate the protective effects of lentivirus mediated Bcl-2-associated athanogene 1L (BAG-1L) over-expression on human neuroblastoma cells (SH-SY5Y) induced by hypoxia/re-oxygenation, and to study its effect on the phosphoinositide 3 kinase serine/threonine protein kinase (PI3K/AKT)
Chronic hypoxia up-regulates expression of adenosine A1 receptors in DDT1-MF2 cells.
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As the first step to understand how chronic hypoxia might regulate smooth muscle function in health and disease, we have employed an established immortalised cell model of smooth muscle, DDT1-MF2 cells, to address the hypothesis that adenosine A1 receptor density is modulated by O2 availability.
Molecular mechanisms of anoxia/reoxygenation-induced neutrophil adherence to cultured endothelial cells.
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The objectives of this study were to (1) determine the time course of neutrophil adhesion to monolayers of human umbilical vein endothelial cells (HUVECs) that were exposed to 60 minutes of anoxia followed by 30 to 600 minutes of reoxygenation and (2) define the mechanisms responsible for both the
Regulation of heme oxygenase-1 gene expression by anoxia and reoxygenation in primary rat hepatocyte cultures.
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Heme oxygenase (HO) catalyzes the rate-limiting enzymatic step of heme degradation and regulates the cellular heme content. Gene expression of the inducible isoform of HO, HO-1, is upregulated in response to various oxidative stress stimuli. To investigate the regulatory role of anoxia and
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