Bacterial lipopolysaccharide antagonizes transforming growth factor β1-induced apoptosis in primary cultures of hepatocytes

Martı́n-Sanz, Paloma; Díaz-Guerra, María José; Casado, Marta

doi:10.1002/hep.510230539

Cited by 19 publications

(12 citation statements)

References 40 publications

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“…GSNO was synthesized from glutathione and NaNO 2 following a previous protocol [14]. GSNO was precipitated with acetone and purified after extensive washing with diethylether.…”

Section: Methodsmentioning

confidence: 99%

“…GSNO was precipitated with acetone and purified after extensive washing with diethylether. After vacuum drying, an aliquot was characterized by UV spectroscopy [14]. NO release was measured by the accumulation of nitrite and nitrate in the culture medium as previously described using Griess reagent [15].…”

Section: Methodsmentioning

confidence: 99%

“…Internucleosomal DNA fragmentation was assessed by distinct independent methods including agarose gel electrophoresis analysis of fragmented DNA, and a cell death ELISA kit (Boehringer) based on the detection of mono‐ and oligonucleosomes in the cytosol [14, 15]. The dishes (1–2×10 6 cells) were washed twice with ice‐cold PBS and lysis was accomplished with 1 ml of 20 mM EDTA, 0.5% Triton X‐100, 5 mM Tris‐HCl, pH 8.0.…”

Section: Methodsmentioning

confidence: 99%

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Requirement of nitric oxide and calcium mobilization for the induction of apoptosis in adrenal vascular endothelial cells

et al. 1997

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“…GSNO was synthesized from glutathione and NaNO 2 following a previous protocol [14]. GSNO was precipitated with acetone and purified after extensive washing with diethylether.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Requirement of nitric oxide and calcium mobilization for the induction of apoptosis in adrenal vascular endothelial cells

et al. 1997

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“…26), we tested the hypothesis that NO regulates apoptosis through nitrosylation of cysteine at the active site of caspase-3-like proteases. We utilized hepatocytes for these studies because we (27)(28)(29) and others (30,31) have shown that NO is hepatoprotective. In addition, hepatocytes express iNOS under a diverse array of conditions associated with cell death and turnover (reviewed in Ref.…”

mentioning

confidence: 99%

Nitric Oxide Inhibits Apoptosis by Preventing Increases in Caspase-3-like Activity via Two Distinct Mechanisms

Kim

Talanian²,

Billiar

1997

Journal of Biological Chemistry

843

668

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Nitric oxide (NO) has emerged as an important endogenous inhibitor of apoptosis, and here we report that NO prevents hepatocyte apoptosis initiated by the removal of growth factors or exposure to TNF␣ or anti-Fas antibody. We postulated that the mechanism of the inhibition of apoptosis by NO would include an effect on caspase-3-like protease activity. Caspase-3-like activity increased coincident with apoptosis due to all three stimuli, and treatment with the caspase-3-like protease inhibitor N-acetyl-Asp-Glu-Val-Asp-aldehyde inhibited both proteolytic activity and apoptosis. Endogenous or exogenous sources of NO prevented the increase in caspase-3-like activity in hepatocytes. Exposure of purified recombinant caspase-3 to an NO or NO ؉ donor inhibited proteolytic activity. Dithiothreitol (DTT), but not glutathione, reversed the inhibition of recombinant caspase-3 by NO. When lysates from cells stimulated to express inducible NO synthase or cells exposed to NO donors were incubated in DTT, caspase-3-like activity increased to about 55% of cells not exposed to a source of NO. Similarly, administration of an NO donor to rats treated with TNF␣ and D-galactosamine also prevented the increase in caspase-3-like activity as measured in liver homogenates. The effect of the NO donor was reversed by about 50% if the homogenate was incubated with DTT. TNF␣-induced apoptosis and caspase-3-like activity were also reduced in cultured hepatocytes exposed to 8-bromo-cGMP, and both effects were inhibited by the cGMP-dependent kinase inhibitor KT5823. The suppression in caspase-3-like activity in hepatocytes exposed to an NO donor was partially blocked by an inhibitor of soluble guanylyl cyclase, 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one, (ODQ), while the incubation of these lysates in DTT almost completely restored caspase-3-like activity to the level of TNF␣-treated controls. These data indicate that NO prevents apoptosis in hepatocytes by either directly or indirectly inhibiting caspase-3-like activation via a cGMP-dependent mechanism and by direct inhibition of caspase-3-like activity through protein S-nitrosylation.Apoptosis, or programmed cell death, is distinguished from lytic or necrotic cell death by specific biochemical and structural events. The apogenic signals trigger specific signaling pathways, including protease activation, which is followed by the appearance of morphologic changes characteristic of cells undergoing apoptosis such as condensation of nuclei and cytoplasm, blebbing of cytoplasmic membranes, and finally fragmentation into apoptotic bodies that are phagocytosed by neighboring cells (reviewed in Ref.

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“…Indeed, it has been reported that NO plays a dual role, favoring cell viability or inducing apoptotic death depending on the cell type and amount of NO produced (11)(12)(13)(14)(15). For example, moderate NO synthesis inhibits basal apoptosis in B lymphocytes (16,17) or the TGF-␤-induced apoptosis in hepatocytes (18).…”

mentioning

confidence: 99%

Sustained Nitric Oxide Delivery Delays Nitric Oxide-Dependent Apoptosis in Macrophages: Contribution to the Physiological Function of Activated Macrophages

Hortelano

Través

Zeini

et al. 2003

The Journal of Immunology

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Treatment of the macrophage cell line RAW 264.7 with the short-lived NO donor S-nitrosoglutathione triggers apoptosis through the release of mitochondrial mediators. However, continuous supply of NO by long-lived NO donors protected cells from apoptosis through mechanisms that involved the maintenance or an increase in the levels of the inhibitor of apoptosis proteins (IAPs) cIAP-1, cIAP-2, and xIAP and decreases in the accumulation of p53 and in the levels and targeting of Bax to the mitochondria. As a result of these changes, the activation of caspases 9 and 3 was notably delayed, expanding the time of viability of the macrophages. Moreover, inhibition of NO synthase 2 activity after 8 h of stimulation of RAW 264.7 cells with LPS and IFN-γ accelerated apoptosis via an increase in the processing and activation of caspases. These data suggest that NO exerts an important role in the autoregulation of apoptosis in macrophages.

show abstract

Bacterial lipopolysaccharide antagonizes transforming growth factor β1-induced apoptosis in primary cultures of hepatocytes

Cited by 19 publications

References 40 publications

Requirement of nitric oxide and calcium mobilization for the induction of apoptosis in adrenal vascular endothelial cells

Requirement of nitric oxide and calcium mobilization for the induction of apoptosis in adrenal vascular endothelial cells

Nitric Oxide Inhibits Apoptosis by Preventing Increases in Caspase-3-like Activity via Two Distinct Mechanisms

Sustained Nitric Oxide Delivery Delays Nitric Oxide-Dependent Apoptosis in Macrophages: Contribution to the Physiological Function of Activated Macrophages

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