In vitro CO2-induced ROS production impairs cell cycle in SH-SY5Y neuroblastoma cells

Montalto, Angela Simona; Currò, Monica; Russo, Tiziana; Visalli, Giuseppa; Impellizzeri, Pietro; Antonuccio, Pietro; Arena, Salvatore; Borruto, Francesca Astra; Scalfari, Gianfranco; Ientile, Riccardo; Romeo, Carmelo

doi:10.1007/s00383-012-3206-3

Cited by 12 publications

(9 citation statements)

References 38 publications

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“…DNA damage was evaluated by using a single‐cell gel electrophoresis technique as previously described (Montalto et al, ). Briefly, after treatment, harvested cells were embedded in a thin agarose gel (1% low melting point) on a microscope slide.…”

Section: Methodsmentioning

confidence: 99%

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

Currò

Salinaro

Koverech

et al. 2014

J of Neuroscience Research

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Recent findings underscore that some natural compounds are responsible for specific biochemical effects, i.e., the activation of redox-sensitive intracellular pathways and modulation of different stress proteins, such as heat shock proteins and sirtuins. Resveratrol, a natural polyphenol widely present in plants, has been shown to display various beneficial effects, including neuroprotection, in several pathological conditions. In the present study, by using differentiated SH-SY5Y neuroblastoma cells, we investigated the potential protective effects of resveratrol against homocysteine-induced neurotoxicity. We observed that homocysteine (100 µM) decreased cell viability while at the same time significantly increasing intracellular reactive oxygen species and DNA fragmentation. Cell pretreatment with resveratrol concentrations ranging from 1 to 5 µM elicited protective effects through the reduction of oxidative stress and genotoxic damage. In addition, we observed that resveratrol produced significant changes in the expression of both Hsp70 and sirtuin 1 (SIRT1). After homocysteine treatment in the presence of resveratrol, SIRT1 protein was found abundantly not only in the cytosol but also in the nucleus, as demonstrated by confocal laser scanning microscopy. The results of this study suggest that resveratrol is a potential protective agent against homocysteine-induced neurotoxicity and that beneficial effects are accompanied by changes in cell stress response. Taken together, these features contribute to our knowledge of underlying mechanisms involved in resveratrol-induced cell survival.

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Section: Methodsmentioning

confidence: 99%

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

Currò

Salinaro

Koverech

et al. 2014

J of Neuroscience Research

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“…Our results showed that in vitro simulated CO 2 pneumoperitoneum environment induces oxidative stress, leading to DNA damage followed by a significant attenuation of cell proliferation mediated by p53 activation. 6 We also reported that CO 2 -induced hypoxic condition exerts cytotoxic effects on NB cells by eliciting mitochondrial apoptotic pathway. 7 It has been well established that cell response to hypoxic stress is mediated by HIFs.…”

Section: Discussionmentioning

confidence: 75%

“…5 The presence of HIF-1α and HIF-2α has been revealed in NB specimens; however, the expression of both proteins did not fully correlate and was dependent on the microenvironment. 18 Although HIF-1 and HIF-2 share common targets involved in many pathways, such as angiogenesis, differentiation, stem cells maintenance, apoptosis, and invasion, 6 it has been previously reported that HIF-1α is associated with a favorable outcome, whereas HIF-2α is implicated in promoting an aggressive NB phenotype correlating with an unfavorable clinical outcome. 19 Our results showed that the exposure of SH-SY5Y NB cells to 15 mm Hg CO 2 (100%) for 4 hours caused an increase in the transcript levels of HIF-1α, which returned to basal levels after 24 hours of incubation in standard condition; in contrast, no changes were observed in the mRNA levels of HIF-2α, suggesting that an acute hypoxic stimulus can be associated with a favorable outcome in our NB cells.…”

Section: Discussionmentioning

confidence: 99%

“…5 Our previous works highlighted several effects caused by CO 2 exposure of NB cells, showing impaired cell cycle and cell apoptosis. 6,7 It has been also reported that, in NB cells, hypoxic stress may induce the overexpression of N-Myc, throughout epigenetic mechanisms, such as the acetylation of H3 and H4 hystones. 8 Several evidences support a positive relationship between hypoxia and angiogenesis, 9 that is a prerequisite for progression and metastatic spread of NB.…”

Section: Introductionmentioning

confidence: 99%

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CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells

et al. 2019

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Introduction CO2 pneumoperitoneum can influence the biological behavior of neuroblastoma (NB). Angiogenesis and genetic features are responsible for malignant phenotype of this tumor. We examined the CO2 effects on N-Myc, vascular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2) expression as critical biomarkers of tumor invasiveness, in NB cells without N-Myc amplification. Materials and Methods SH-SY5Y cells were exposed to CO2 (100%) at 15 mm Hg pressure for 4 hours and then moved to normal condition for 24 hours. Control cells were incubated with 5% CO2 for the same time. In control and CO2-exposed cells, the messenger ribonucleic acid (mRNA) levels of hypoxia-inducible factor (HIF)-1α, HIF-2α, VEGF-A, and MMP-2 were quantified by real-time polymerase chain reaction. N-Myc expression was evaluated by Western blot analysis. Results The exposure to 15 mm Hg CO2 (100%) for 4 hours induced an increase in HIF-1α, but not in HIF-2α, mRNA levels. No differences were observed in N-Myc expression between exposed and control cells at each incubation time. Similarly, no significant differences were found for VEGF-A and MMP-2 transcript levels. In CO2 exposed cells, we observed only a slight increase in both VEGF-A and MMP-2 mRNA levels after 4 and 24 hours in comparison to controls. Conclusion In our study, the hypoxic environment induced by CO2 exposure does not affect the expression of critical biomarkers of NB aggressiveness, such as N-Myc, VEGF, and MMP-2, in human SH-SY5Y NB cells without N-Myc amplification. These data suggest that CO2 pneumoperitoneum might not adversely impact NB cell invasiveness; however, it is necessary to evaluate these effects in others in vitro and in vivo models.

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“…At the cellular level, CO 2 -induces changes in pH and may alter neuronal excitability by altering extracellular adenosine and ATP concentrations (Xu, Uh et al, 2011). CO 2 insufflation-induces oxidative stress and has a toxic effect on neuroblastoma cells leading to DNA damage (Montalto, Currò et al, 2013). In E. coli, CO 2 was seen to exacerbate the toxicity of ROS in a dose-dependent manner (Ezraty, Ducret et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

PRL-1 is required for neuroprotection against olfactory CO₂ stimulation in Drosophila

Yang

Guo

et al. 2018

Preprint

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The Mammalian phosphatase of regenerating liver (PRL) family is primarily recognized for its oncogenic properties. Here we found that in Drosophila, loss of prl-1 resulted in CO2-induced brain disorder presented as irreversible wing hold up with enhancement of Ca2+ responses at the neuron synaptic terminals. Overexpression of Prl-1 in the nervous system could rescue the mutant phenotype. We show that Prl-1 is particularly expressed in CO2-responsive neural circuit and the higher brain centers.Ablation of the CO2 olfactory receptor, Gr21a, suppressed the mutant phenotype, suggesting that CO2 acts as a neuropathological substrate in absence of Prl-1. Further studies found that the wing hold up is an obvious consequence upon knockdown of Uex, a magnesium transporter, which directly interacts with Prl-1. Conditional expression of Uex in the nervous system could rescue the phenotype of prl-1 mutants. We demonstrate that Uex acts genetically downstream of Prl-1. Our findings provide important insights into mechanisms of Prl-1 protection against olfactory CO2 stimulation induced brain disorder at the level of detailed neural circuits and functional molecular connections.

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In vitro CO2-induced ROS production impairs cell cycle in SH-SY5Y neuroblastoma cells

Abstract: In vitro-simulated pneumoperitoneum environment with CO(2) induces oxidative stress and cell DNA damage, leading to p53 up-regulation involved in cell-cycle arrest of neuroblastoma cells.

Cited by 12 publications

References 38 publications

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells

PRL-1 is required for neuroprotection against olfactory CO₂ stimulation in Drosophila

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In vitro CO2-induced ROS production impairs cell cycle in SH-SY5Y neuroblastoma cells

Abstract: In vitro-simulated pneumoperitoneum environment with CO(2) induces oxidative stress and cell DNA damage, leading to p53 up-regulation involved in cell-cycle arrest of neuroblastoma cells.

Cited by 12 publications

References 38 publications

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

Resveratrol protects against homocysteine‐induced cell damage via cell stress response in neuroblastoma cells

CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells

PRL-1 is required for neuroprotection against olfactory CO2 stimulation in Drosophila

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PRL-1 is required for neuroprotection against olfactory CO₂ stimulation in Drosophila