1,721,058 research outputs found
Escherichia-coli lipopolysaccharide enhances the release of a no-like factor from astrocytoma-cells in culture
No full textAn 18 h coincubation of a human astrocytoma cell line (GO-G-UVW) with E. coli lipopolysaccharide (LPS) significantly increased nitrite concentrations in cell culture medium and potentiated the inhibition of human washed thrombin-induced platelet aggregation produced solely by astrocytoma cells. This was due to the increased release from astrocytoma cells of nitric oxide (NO) or a NO-like substance, since it was prevented by oxyhemoglobin (OxyHb), a trapping agent for NO, and potentiated by superoxide dismutase (SOD), which enhances the biological effects of NO through the removal of superoxide anions. In addition, the NO-like factor released by astrocytoma cells seems to originate from L-arginine, since its anti-aggregatory properties, as well as nitrite generation in astrocytoma cells culture medium, were blocked by incubating cells with N(G)-monomethyl-L-arginine, a selective inhibitor of NO synthase. These effects were restored by L-arginine, the precursor of NO, but not by D-arginine. In conclusion, the present experiments show that LPS is able to increase the release of NO or a NO-like substance from glial cells and suggest that, under conditions in which high levels of endotoxin are present (septic shock, severe infections), or under some pathological conditions accompanied by an abnormal permeability of the blood brain barrier, NO released from glial cells may affect neuronal activity in the brain
BACTERIAL LIPOPOLISACCARIDE PLUS INTERFERON-gamma ELICIT A VERY FAST INHIBITION OF A CA-DEPENDENT NITRIC-OXIDE SYNTHASE ACTIVITY IN HUMAN ASTROCYTOMA CELLS
No full textHIV coating gp 120 glycoprotein-dependent prostaglandin E2 release by human cultured astrocytoma cells is regulated by nitric oxide formation
No full textAnimal models of cardiac cachexia
No full textCachexia is the loss of body weight associated with several chronic diseases including chronic heart failure (CHF). The cachectic condition is mainly due to loss of skeletal muscle mass and adipose tissue depletion. The majority of experimental in vivo studies on cachexia rely on animal models of cancer cachexia while a reliable and appropriate model for cardiac cachexia has not yet been established.
A critical issue in generating a cardiac cachexia model is that genetic modifications or pharmacological treatments impairing the heart functionality and used to obtain the heart failure model might likely impair the skeletal muscle, this also being a striated muscle and sharing with the myocardium several molecular and physiological mechanisms. On the other hand, often, the induction of heart damage in the several existing models of heart failure does not necessarily lead to skeletal muscle loss and cachexia.
Here we describe the main features of cardiac cachexia and illustrate some animal models proposed for cardiac cachexia studies; they include the genetic calsequestrin and Dahl salt-sensitive models, the monocrotaline model and the surgical models obtained by left anterior descending (LAD) ligation, transverse aortic constriction (TAC) and ascending aortic banding.
The availability of a specific animal model for cardiac cachexia is a crucial issue since, besides the common aspects of cachexia in the different syndromes, each disease has some peculiarities in its etiology and pathophysiology leading to cachexia. Such peculiarities need to be unraveled in order to find new targets for effective therapies
HIF-1, the Warburg Effect, and Macrophage/Microglia Polarization Potential Role in COVID-19 Pathogenesis
Full text linkDespite the international scientific community's commitment to improve clinical knowledge about coronavirus disease 2019 (COVID-19), knowledge regarding molecular details remains limited. In this review, we discuss hypoxia's potential role in the pathogenesis of the maladaptive immune reaction against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The state of infection, with serious respiratory dysfunction, causes tissues to become hypoxic due to a discrepancy between cellular O2 uptake and consumption similar to that seen within tumor tissue during the progression of numerous solid cancers. In this context, the heterogeneous clinical behavior and the multiorgan deterioration of COVID-19 are discussed as a function of the upregulated expression of the hypoxia-inducible factor-1 (HIF-1) and of the metabolic reprogramming associated with HIF-1 and with a proinflammatory innate immune response activation, independent of the increase in the viral load of SARS-CoV-2. Possible pharmacological strategies targeting O2 aimed to improve prognosis are suggested
Bacterial Lipopolysaccharide plus interferon -γ elicit a very fast inhibition of a Ca2+-dependent nitric-oxide synthase activity in human astrocytoma cells
No full textPrevious results indicate that induction of inducible nitric-oxide synthase (iNOS) expression may be kept suppressed by the endogenous NO level as produced by a constitutive NOS (cNOS) enzyme. In cell types possessing both cNOS and iNOS, this may represent an evident paradox. Here, we report that lipopolysaccharide and interferon-γ, which are able to strongly induce iNOS in astrocytoma cells, can rapidly inhibit the NO production generated by the constitutive NOS isoform, thus obtaining the best conditions for iNOS induction and resolving the apparent paradox. In fact, a 30-rain treatment of T67 cells with the combination of lipopolysaccharide plus interferon-γ (MIX) strongly inhibits the cNOS activity, as determined by measuring [3H]citrulline production. In addition, the effect of MIX is also observed by measuring nitrite, the stable breakdown product of NO: a 30-min pretreatment of T67 cells with MIX is able to reduce significantly the N- methyl-D-aspartate-induced nitrite production. Finally, using reverse transcriptase-polymerase chain reaction, we have observed that a 30-min treatment of T67 cells with MIX does not affect expression of mRNA coding for the neuronal NOS-I isoform. These results suggest the novel concept of a possible role of a cNOS isoform in astrocytes as a control function on iNOS induction
HIV gp 120 glycoprotein stimulates the inducible isoform of NO syntase in human cultured astrocytoma cells
No full textHIV gp120 glycoprotein stimulates the inducible isoform of no synthase in human cultured astrocytoma cells
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