SNAP, a NO donor, induces cortical neuron death by a mechanism in which the caspase pathway is implicated

Figueroa, Sara Manzano; Cañadas, S.; Arce, Carmen; Oset-Gasque, María Jesús; González, M.P.

doi:10.1016/j.brainres.2005.04.044

Cited by 7 publications

(6 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, at higher concentrations, it can be neurotoxic (Gross and Wolin, 1995;Dawson and Dawson, 1996;Figueroa et al, 2005b) and may be implicated in several pathologi-cal processes, such as brain ischemia and neurodegeneration (Jenner and Olanow, 1996;Murphy, 1999;Jellinger and Stadelmann, 2000). In the present study, we demonstrate that S-nitroso-N-acetylpenicillamine (SNAP), a NO donor, at concentrations higher than 10 lM, induces death in cortical neurons.…”

mentioning

confidence: 76%

Mitochondrial involvement in nitric oxide‐induced cellular death in cortical neurons in culture

Figueroa

Oset-Gasque

Arce

et al. 2006

J of Neuroscience Research

Self Cite

View full text Add to dashboard Cite

Nitric oxide (NO) is an unstable molecule with physiological and pathological properties. In brain, NO acts as a modulator of neurotransmission as well as a protector against neuronal death from several death stimuli. However, beside this protector effect, high NO concentrations produce neuronal death by a mechanism in which the caspase pathway is implicated. In this work, we demonstrate that in cortical neurons the NO toxicity is mediated by mitochondrial dysfunction. SNAP, an NO donor, induces apoptosis in these cells because it 1) increases the p53 and 2) induces cytochrome c release and activation of caspase-9 and caspase-3. SNAP also induces necrosis, through 1) breakdown of the mitochondrial membrane potential, 2) ATP decrease, 3) ROS formation, and 4) LDH and ATP release, indicative of oxidative stress and death by necrosis. To sum up, in cortical neurons, high NO concentrations produced cellular death by both an apoptotic and a necrotic mechanism in which the mitochondria are implicated.

show abstract

mentioning

confidence: 76%

Mitochondrial involvement in nitric oxide‐induced cellular death in cortical neurons in culture

Figueroa

Oset-Gasque

Arce

et al. 2006

J of Neuroscience Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Control of the caspase pathway during oxidative stress may be vital to provide protection against PCD (Figueroa, S et al, 2005, Paucard, A et al, 2004. The caspases 1 and 3 have each been linked to the independent apoptotic pathways of genomic DNA cleavage and cellular membrane PS exposure , Chong, ZZ et al, 2003e, Takahashi, H et al, 1999.…”

Section: The "Extrinsic and Intrinsic" Pathways Of The Mglur Systemmentioning

confidence: 98%

Driving Cellular Plasticity and Survival Through the Signal Transduction Pathways of Metabotropic Glutamate Receptors

Maiese¹,

Chong²,

Li³

2005

CNR

View full text Add to dashboard Cite

Metabotropic glutamate receptors (mGluRs) share a common molecular morphology with other G protein-linked receptors, but there expression throughout the mammalian nervous system places these receptors as essential mediators not only for the initial development of an organism, but also for the vital determination of a cell's fate during many disorders in the nervous system that include amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, Multiple Sclerosis, epilepsy, trauma, and stroke. Given the ubiquitous distribution of these receptors, the mGluR system impacts upon neuronal, vascular, and glial cell function and is activated by a wide variety of stimuli that includes neurotransmitters, peptides, hormones, growth factors, ions, lipids, and light. Employing signal transduction pathways that can modulate both excitatory and inhibitory responses, the mGluR system drives a spectrum of cellular pathways that involve protein kinases, endonucleases, cellular acidity, energy metabolism, mitochondrial membrane potential, caspases, and specific mitogen-activated protein kinases. Ultimately these pathways can converge to regulate genomic DNA degradation, membrane phosphatidylserine (PS) residue exposure, and inflammatory microglial activation. As we continue to push the envelope for our understanding of this complex and critical family of metabotropic receptors, we should be able to reap enormous benefits for both clinical disease as well as our understanding of basic biology in the nervous system.

show abstract

“…SNAP, an NO donor, is generally regarded as a pro‐apoptotic stimulus in non‐neuronal [21–23] and neuronal cell lines [20, 24]. It has been well documented that SNAP‐mediated apoptosis is associated with the activation of caspase‐3 and poly‐ADP‐ribose polymerase (PARP) in the intrinsic apoptosis pathway.…”

Section: Resultsmentioning

confidence: 99%

“…S ‐nitroso‐ N ‐acetylpenicillamine (SNAP) was prepared according to Figueroa et al. [20]; cells were treated with SNAP for 24 hr, and melatonin was added 10 hr prior to SNAP treatment.…”

Section: Methodsmentioning

confidence: 99%

Melatonin prevents nitric oxide‐induced apoptosis by increasing the interaction between 14‐3‐3β and p‐Bad in SK‐N‐MC cells

Choi

Joo

Yoo

2007

Journal of Pineal Research

View full text Add to dashboard Cite

The anti-apoptotic effect of melatonin has been described in vivo and in vitro. A previous report has revealed that melatonin suppresses nitric oxide (NO)-induced apoptosis via the induction of Bcl-2 expression in PGT-beta pineal cells. To investigate the protective mechanism of melatonin on NO donor S-nitroso-N-acetyl-penicillamine (SNAP)-induced apoptosis, we examined the anti-apoptotic upstream signaling pathway of Bcl-2 in the human neuroblastoma cell line SK-N-MC. The flow cytometry results revealed that apoptosis occurred in NO-treated cells, while cell death was inhibited by pretreatment with melatonin (100 microm). In addition, decreased Bax expression, increased Bcl-2 expression and a decreased release of cytochrome c into the cytosol were observed in the melatonin-pretreated SK-N-MC cells. We also found that melatonin treatment induced the activation of Akt/PKB and the phosphorylation of GSK3alpha/beta and Bad. Furthermore, melatonin treatment not only increased the protein-protein interactions between 14-3-3beta and p-Bad, but also decreased the release of cytochrome c from mitochondria into the cytosol. In summary, the protective effect of melatonin against NO-induced apoptosis was mediated by the inhibition of Bad translocation from the cytosol to the mitochondria by the induction of protein-protein interactions between 14-3-3beta and p-Bad.

show abstract

SNAP, a NO donor, induces cortical neuron death by a mechanism in which the caspase pathway is implicated

Cited by 7 publications

References 16 publications

Mitochondrial involvement in nitric oxide‐induced cellular death in cortical neurons in culture

Mitochondrial involvement in nitric oxide‐induced cellular death in cortical neurons in culture

Driving Cellular Plasticity and Survival Through the Signal Transduction Pathways of Metabotropic Glutamate Receptors

Melatonin prevents nitric oxide‐induced apoptosis by increasing the interaction between 14‐3‐3β and p‐Bad in SK‐N‐MC cells

Contact Info

Product

Resources

About