Autologous nitric oxide protects mouse and human keratinocytes  from ultraviolet B radiation-induced apoptosis

Weller, Richard; Schwentker, Ann; Billiar, Timothy R.; Vodovotz, Yoram

doi:10.1152/ajpcell.00462.2002

Cited by 71 publications

(53 citation statements)

References 53 publications

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“…For example, eNOS inhibits tumor necrosis factor-related apoptosisinducing ligand-induced and ROS-induced apoptosis in prostate tumor cells (24,25). Others have found that eNOS can decrease apoptosis and increase survival through the Bcl-2 (26) and soluble guanylate cyclase (sGC)/cGMP pathways (27). In addition, eNOS has a p53-binding site.…”

Section: Enos and Apoptosismentioning

confidence: 99%

An Emerging Role for Endothelial Nitric Oxide Synthase in Chronic Inflammation and Cancer

2007

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Section: Enos and Apoptosismentioning

confidence: 99%

An Emerging Role for Endothelial Nitric Oxide Synthase in Chronic Inflammation and Cancer

2007

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“…In human thymocytes [28] and neutrophiles [29], NO induces apoptosis, while it inhibits cell death in human keratinocytes [30] and hepatocytes [31]. Some studies provided conclusive evidence that NO is a potent inhibitor of caspase activity both in vitro and in vivo [32], demonstrating that NO suppresses apoptosis signaling by S-nitrosylation of active site cysteine of the caspases, as caspase-3 [33] and capase-1 [34].…”

Section: Introductionmentioning

confidence: 99%

Evidence for the role of nitric oxide in antiapoptotic and genotoxic effect of nicotine on human gingival fibroblasts

Argentin

Cicchetti

2006

Apoptosis

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Resistance to apoptosis is essential for cancer survival and plays a critical role in carcinogenesis. Growing evidence suggests that nicotine can act as a tumor promoter, impairing apoptotic process in certain types of human cancer cell lines. Our previous study revealed in human gingival fibroblasts (HGFs) a concomitant antiapoptotic and genotoxic effect of nicotine, manifested by the attenuation of staurosporine (STP)-induced apoptosis and the increase of micronucleus frequency. The present report provides evidence that nitric oxide (NO) is critically involved in these actions. In vitro treatment with sodium nitroprusside as NO donor showed that NO produced similar effects as those observed with nicotine: it caused DNA damage and partially prevented apoptosis induced by staurosporine. Exposure of HGFs to nicotine, at concentrations similar to those found in the blood of habitual smokers, leads to the production of NO associated with the induction of inducible nitric oxide synthase (iNOS) expression. Experiments using an inhibitor of iNOS, N-monomethyl-L-arginine (NMA), together with nicotine confirmed the involvement of NO in the drug action, abrogating completely cell death and a good part of the genotoxicity. Finally, we show by different approaches that the inhibition of cell death by nicotine through NO release is related to modulation of caspase-1 activation.

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“…To prove this hypothesis, we assessed the effect of a NO do-nor, S-Nitroso-N-acetylpenicillamine (SNAP), on the nonhypoxic induction of HIF-1α and the VEGF production in cardiomyocytes, using the primary cultured rat cardiomyocytes (PRCMs). munoblotting assay [21,22]. Cardiomyocytes were pretreated with one of these agents prior to the addition of SNAP.…”

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confidence: 99%

Nitric Oxide Stimulates Vascular Endothelial Growth Factor Production in Cardiomyocytes Involved in Angiogenesis

et al. 2006

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Background: Hypoxia-inducible factor (HIF)-1α regulates the transcription of lines of genes, including vascular endothelial growth factor (VEGF), a major gene responsible for angiogenesis. Several recent studies have demonstrated that a nonhypoxic pathway via nitric oxide (NO) is involved in the activation of HIF-1α. However, there is no direct evidence demonstrating the release of angiogenic factors by cardiomyocytes through the nonhypoxic induction pathway of HIF-1α in the heart. Therefore we assessed the effects of an NO donor, S-Nitroso-N-acetylpenicillamine (SNAP) on the induction of VEGF via HIF-1α under normoxia, using primary cultured rat cardiomyocytes (PRCMs). Methods and Results: PRCMs treated with acetylcholine (ACh) or SNAP exhibited a significant production of NO. SNAP activated the induction of HIF-1α protein expression in PRCMs during normoxia. Phosphatidylinositol 3-kinase (PI3K)-dependent Akt phosphorylation was induced by SNAP and was completely blocked by wortmannin, a PI3K inhibitor, and N G -nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor. The SNAP treatment also increased VEGF protein expression in PRCMs. Furthermore, conditioned medium derived from SNAP-treated cardiomyocytes phosphorylated the VEGF type-2 receptor (Flk-1) of human umbilical vein endothelial cells (a fourfold increase compared to the control group, p < 0.001, n = 5) and accelerated angiogenesis. Conclusion: Our results suggest that cardiomyocytes produce VEGF through a nonhypoxic HIF-1α induction pathway activated by NO, resulting in angiogenesis.

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Autologous nitric oxide protects mouse and human keratinocytes from ultraviolet B radiation-induced apoptosis

Cited by 71 publications

References 53 publications

An Emerging Role for Endothelial Nitric Oxide Synthase in Chronic Inflammation and Cancer

An Emerging Role for Endothelial Nitric Oxide Synthase in Chronic Inflammation and Cancer

Evidence for the role of nitric oxide in antiapoptotic and genotoxic effect of nicotine on human gingival fibroblasts

Nitric Oxide Stimulates Vascular Endothelial Growth Factor Production in Cardiomyocytes Involved in Angiogenesis

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