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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to examine the mechanisms of thapsigargin-induced apoptosis in rat glomerular mesangial cells and the possible involvement of nitric oxide (NO) in this process. In mesangial cell monolayers incubated for 12 h in a medium without growth factors and with 10(-6) M thapsigargin, a known specific inhibitor of endoplasmic reticulum Ca(2+)-ATPase, a high percentage of cells showed typical nuclear features of apoptosis, assessed either by staining with propidium iodide (23 vs. 9% in control conditions) or by terminal desoxynucleotidyl transferase-mediated dUTP biotin nick end labelling (TUNEL; 17 vs. 5% in control conditions). When cells were maintained in a medium containing 10% fetal calf serum (FCS) or in a free-calcium medium, the thapsigargin-induced apoptosis rate was very low. In rat mesangial cells treatment with thapsigargin decreased the expression of BCL-2 protein and bcl-2 mRNA, whereas it did not alter the levels of BAX protein or bax mRNA. When mesangial cells were incubated with thapsigargin in the absence of FCS, we detected a significant increase in nitrite production (3.78 +/- 0.96 vs. 1.76 +/- 0.44 micromol/well). Furthermore, the treatment with the NO synthesis inhibitor L-NAME (10(-4) M) induced a significant decrease in the number of apoptotic cells (9%), whereas incubation with the NO donor SIN-1 (10(-5) M) induced a marked increase in the rate of apoptosis (29%). Western and Northern blot analysis of macrophage-type inducible NO synthase (iNOS) demonstrated that thapsigargin treatment induces the expression of the iNOS protein and iNOS mRNA. Treatment with L-NAME prevented the thapsigargin-induced BCL-2 decrease, whereas incubation with SIN-1 potentiated the effect of thapsigargin on BCL-2. Double labelling by immunohistochemistry for iNOS and TUNEL revealed that the same cells that suffered apoptosis were positive for iNOS. In summary, our results indicate that thapsigargin is able to enhance the apoptosis rate of rat mesangial cells by a mechanism that is mediated by an increase in cytosolic free calcium. Increased iNOS expression, and hence increased NO production, seems to be involved in this effect.
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PMID:Nitric oxide is involved in apoptosis induced by thapsigargin in rat mesangial cells. 1074 95

The effects of different doses of nitric oxide (NO) on the proliferation and apoptosis of the cultured bovine trabecular meshwork (TM) cells were studied. L-arginine and NG-nitro-L-arginine methyl (L-NAME) were incubated with TM cells for 48 h. In the control group, no medicine was given. In the experimental groups, concentrations of L-arginine and L-NAME were 1 x 10(-7) mol/L, 1 x 10(-6) mol/L, 1 x 10(-5) mol/L, 1 x 10(-4) mol/L, 1 x 10(-3) mol/L and 1 x 10(-2) mol/L, respectively. NO2- in supernate, the proliferation and apoptosis of TM cells and mRNA expression of bcl-2 and bax were measured by Griess reagent, terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), MTT assay and in situ hybridization, respectively. The results showed that L-arginine with concentration > or = 1 x 10(-4) mol/L could induce apoptosis of the TM cells and inhibit the proliferation of TM cells through increasing the NO levels, down-regulating bcl-2 mRNA expression and up-regulating bax mRNA expression; L-NAME with concentration > or = 1 x 10(-5) mol/L could induce the proliferation of the TM cells through suppressing the production of NO. It was concluded that NO in high level could induce apoptosis of the TM cells and suppress the proliferation of the TM cells.
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PMID:Effects of nitric oxide on proliferation and apoptosis of cultured bovine trabecular meshwork cells. 1265 90

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

Autoantibodies against recoverin, a Ca2+-binding protein found in patients with cancer-associated retinopathy (CAR syndrome), penetrate retinal cells and induce their apoptosis via a mitochondrial pathway. The goal of this study was to investigate whether the entry of anti-recoverin antibody into E1A.NR3 retinal cells causes a change in intracellular Ca2+. Intracellular Ca2+ was measured using the Ca2+-sensitive fluorescent dye Fura-2 AM in living E1A.NR3 retinal cells treated with anti-recoverin antibody Rec-1, patients' autoantibodies, and control rat and human IgG. The exposure of retinal cells to Rec-1 antibody and to the CAR patients' autoantibodies in vitro caused a significant increase in intracellular Ca2+, while non-specific antibodies did not induce such an effect. Co-treatment of the E1A.NR3 cells with Rec-1 in the presence of nifedipine, a L-type Ca2+ channel blocker, significantly suppressed the increase of Ca2+. Treatment with nifedipine also blocked changes in the anti-apoptotic protein bcl-xL and in expressions of the pro-apoptotic protein bax. Nifedipine-treated cells also showed a decrease in cytosolic cytochrome c release and a decrease in caspase 3 activation, compared to cells treated only with Rec-1 antibody. The increase in the antibody-induced Ca2+ is at least in part dependent on extracellular Ca2+. Nifedipine was found to inhibit the entry of Ca2+ into the cells and to protect them from Rec-1-induced apoptosis. Increased levels of intracellular Ca2+ may lead to retinal dysfunction and degeneration in the CAR syndrome. Our results provide a molecular basis for the use of Ca2+ blockers in the treatment of the CAR syndrome.
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PMID:Anti-recoverin antibodies induce an increase in intracellular calcium, leading to apoptosis in retinal cells. 1642 15