Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased levels of serum IgE have been described in HIV-1 infection; however, mechanisms implicated in this immunoglobulin production remain unknown. In this study, we demonstrate that in vitro infection of human peripheral blood mononuclear cells (PBMCs) by HIV-1 monocytotropic (Ba-L) or lymphocytotropic (LAI) strains promotes IL-4-induced IgE production, indicating that the HIV-1 infectious process may participate in the IgE production observed in vivo. The effect of membrane glycoproteins (gp160, gp120, and gp41) was also evaluated. It was found that gp120 specifically potentiates in a dose-dependent manner IL-4-induced IgE production and does not affect IL-4-induced IgG, IgA, or IgM production. In these experiments, gp160 was also found to upregulate IL-4-induced IgE production, whereas gp41 was ineffective. This effect of gp120, gp160, and HIV-1 infection on IgE synthesis was not observed in the absence of IL-4. In the presence of IL-4, the inducing effect of gp120 appeared to be indirect because gp120 did not modify purified B lymphocyte IgE production after IL-4 and anti-CD40 monoclonal antibody stimulation. As HIV-1 infection is associated with alterations of PBMC redox metabolism, the role of nitric oxide (NO) in this IgE production by human PBMCs was evaluated. In the presence of a specific inhibitor of NO synthase pathways (L-NAME), IgE production induced by IL-4 and gp120 was abolished. Taken together, these data indicate that HIV-1 envelope glycoprotein gp120 (and gp160) specifically enhances IL-4-induced IgE production by normal human PBMCs, probably through the regulation of the nitric oxide pathway.
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PMID:Role of nitric oxide in the promoting effect of HIV type 1 infection and of gp120 envelope glycoprotein on interleukin 4-induced IgE production by normal human mononuclear cells. 1071 Feb 13

Chronic inhibition of nitric oxide synthase promotes renin-dependent hypertension and renal injury. The present study examines how renal angiotensin II receptors are expressed in this model. N(G)-nitro-L-arginine methyl ester (L-NAME) was given orally to rats for 1 month and was associated or not with captopril during the 4 last days of the administration. 125I-[Sar1, Ile8]-Ang II binding, AT1)mRNA and cytosolic calcium were studied in isolated glomeruli from L-NAME and control rats and in cultured mesangial cells from normal rats. Renal injury was marked in rats receiving L-NAME. Type I angiotensin II (AT1) receptor number and mRNA expression were decreased (p < 0.05) in glomeruli isolated from L-NAME-treated rats compared with controls, unless they received captopril in combination. The low level of AT1 receptor expression was associated with an attenuated rise of cytosolic calcium in response to angiotensin II. Angiotensin-converting enzyme activity in glomeruli and angiotensin II concentration in renal cortex were increased (p < 0.05) in rats receiving L-NAME alone, whereas aminopeptidase A activity was not modified. To better discriminate between the direct and indirect effects of nitric oxide deficiency, rat mesangial cells were exposed or not for 24 h to S-nitroso-N-acetyl penicillamine, a nitric oxide donor. Angiotensin II binding, AT1 mRNA expression and calcium response to angiotensin II were decreased in presence of the nitric oxide donor (p < 0.01). These results suggest that the decrease of AT1 receptor expression after 1 month of L-NAME treatment does not depend on a direct effect of nitric oxide deficiency but results from the high local angiotensin II concentration due to the stimulated angiotensin-converting enzyme activity. They also show that the renin-angiotensin dependence of this model of hypertension does not result from the overexpression of AT1 receptors.
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PMID:AT1 receptor expression in glomeruli from NO-deficient rats. 1464 64

We studied the effect of HIV-1 gp160 protein and morphine on murine macrophage and human monocyte apoptosis. gp160 not only promoted murine macrophage apoptosis but also enhanced macrophage iNOS expression/NO generation. gp160 also altered macrophage bax and bcl-2 expression. Morphine enhanced (P<0.001) the effect of gp160 on macrophage apoptosis as well as iNOS expression/NO generation. Nevertheless, both morphine- and gp160-induced murine macrophage apoptosis was attenuated by nitric oxide synthase (NOS) inhibitors (L-NAME and L-NMMA). On the other hand, free radical scavengers such as superoxide dismutase (SOD), dimethylthiourea (DMTU) and catalase attenuated morphine and gp160-induced human monocyte apoptosis.
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PMID:Morphine modulates HIV-1 gp160-induced murine macrophage and human monocyte apoptosis by disparate ways. 1497 89

The effect of angiotensin (Ang)-1-7 on dopamine, gamma-aminobutyric acid (GABA) and glutamate release in the striatum of the rat was examined using in vivo microdialysis. Ang-(1-7) was administered locally in the striatum through the microdialysis probe. At a concentration of 100 microm, Ang-(1-7) caused a significant increase in extracellular dopamine and GABA but had no effect on glutamate release. The Ang-(1-7)-induced dopamine release was blocked by EC33, an inhibitor of aminopeptidase A, an enzyme which converts Ang-(1-7) into Ang-(3-7), suggesting that this effect occurs after metabolism into Ang-(3-7). Indeed, administration of Ang-(3-7) (10-100 microm) into the striatum caused a more potent increase in the striatal dopamine release than Ang-(1-7). Because Ang-(3-7) is an inhibitor of insulin-regulated aminopeptidase (IRAP) and because Ang IV, another IRAP inhibitor, also causes a concentration-dependent increase in dopamine in the rat striatum, IRAP may be involved in this effect. In contrast, EC33 had no effect on the Ang-(1-7)-induced GABA increase but the GABA release was blocked by the putative AT(1-7) receptor antagonist A779 (0.1 microm) and by the nitric oxide synthase inhibitor L-NAME (1 mm). These drugs could not block the effect of Ang-(1-7) on the striatal dopamine release suggesting that only the observed effects on GABA release are mediated by the AT(1-7) receptor and/or are associated with a release of nitric oxide.
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PMID:In vivo characterization of the angiotensin-(1-7)-induced dopamine and gamma-aminobutyric acid release in the striatum of the rat. 1610 47

Suicide is a leading cause of mortality worldwide. Dysregulated hypothalamic-pituitary-adrenal (HPA) axis activity, as measured by cortisol levels, has been identified as 1 potential risk factor. Evidence has indicated that childhood trauma is associated with dysregulated cortisol reactivity to stress in adulthood. The current study investigated for the first time whether childhood trauma and daily stressors and emotions were associated with diurnal cortisol levels over a 7-day study in individuals vulnerable to suicide. One hundred and forty-two participants were categorized according to their suicidal history into 3 groups: suicide attempt, suicidal ideation, or control group. Participants completed questionnaires before commencing a 7-day study. Cortisol samples were provided immediately upon waking, at 15 min, 30 min, 45 min, 3 hr, 6 hr, 9 hr, and 12 hr on 7 consecutive days. Measures of daily stressors, mood, defeat, and entrapment were completed at the end of each day. Participants in the suicide attempt and ideation groups released significantly lower cortisol upon awakening (CAR) and had a tendency toward flatter wake-peak to 12 hr (WP-12) cortisol slopes compared to controls. Childhood trauma was found to be associated with significantly lower CAR and a tendency toward flatter WP-12 cortisol slope. Childhood trauma also had an indirect effect on suicide vulnerability group membership via lower daily CAR levels. Lower CAR was associated with increased suicide ideation at 1 month but not 6 months. Daily stress and emotion measures were not associated with cortisol levels. This is the first 7-day daily diary investigation of naturally fluctuating cortisol levels in individuals vulnerable to suicide. The results indicate that dysregulated HPA axis activity is associated with suicidal ideation and behavior. Childhood trauma appears to be an important distal factor associated with HPA-axis dysregulation. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
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PMID:Effects of childhood trauma, daily stress, and emotions on daily cortisol levels in individuals vulnerable to suicide. 3165 98