Protective effect of suramin against cell death in rat cerebellar granular neurons and mouse neuroblastoma cells

Bezvenyuk, Zinaida; Suuronen, Tiina; Salminen, Antero; Solovyan, V. T.

doi:10.1016/s0304-3940(00)01453-1

Cited by 7 publications

(5 citation statements)

References 21 publications

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“…This is in contrast to results obtained in rat cerebellar granular neurons undergoing apoptosis in response to glutamate (Bezvenyuk et al 2000) or dequalinium (Chan and Lin-Shiau, 2000), mouse neuroblastoma cells treated with staurosporine (Bezvenyuk et al, 2000), or human hepatic or T cell lines following Fas ligation (Eichhorst et al, 2004). This is in contrast to results obtained in rat cerebellar granular neurons undergoing apoptosis in response to glutamate (Bezvenyuk et al 2000) or dequalinium (Chan and Lin-Shiau, 2000), mouse neuroblastoma cells treated with staurosporine (Bezvenyuk et al, 2000), or human hepatic or T cell lines following Fas ligation (Eichhorst et al, 2004).…”

Section: Discussioncontrasting

confidence: 99%

“…Futhermore, Fas induced apoptotic liver damage was attenuated by suramin (Eichhorst et al, 2004). In addition, a neuroprotective effect of suramin has been described in rat cerebellar granule cells, mouse neuroblastoma cells and in a model of cerebral ischemia (Bezvenyuk et al, 2000;Kharlamov et al, 2002). In addition, a neuroprotective effect of suramin has been described in rat cerebellar granule cells, mouse neuroblastoma cells and in a model of cerebral ischemia (Bezvenyuk et al, 2000;Kharlamov et al, 2002).…”

Section: Suramin Induces and Enhances Apoptosis In A Modelmentioning

confidence: 95%

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Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

et al. 2008

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Recent evidence suggests oxygen as a powerful trigger for cell death in the immature white matter, leading to periventricular leukomalacia (PVL) as a cause of adverse neurological outcome in survivors of preterm birth. This oligodendrocyte (OL) death is associated with oxidative stress, upregulation of apoptotic signaling factors (i.e., Fas, caspase-3) and decreased amounts of neurotrophins. In search of neuroprotective strategies we investigated whether the polysulfonated urea derivative suramin, recently identified as a potent inhibitor of Fas signaling, affords neuroprotection in an in vitro model of hyperoxia-induced injury to immature oligodendrocytes. Immature OLs (OLN-93) were subjected to 80% hyperoxia (48 h) in the presence or absence of suramin (0, 30, 60, 120 microM). Cell death was assessed by flow cytometry (Annexin V, caspase-3 activity assay) and immunohistochemistry for activated caspase-3. Immunoblotting for the death receptor Fas, cleaved caspase-8 and the phosphorylated isoform of the serine-threonin kinase Akt (pAkt) was performed. Suramin lead to OL apoptosis and potentiated hyperoxia-induced injury in a dose-dependent manner. Immunoblotting revealed increased Fas and caspase-8 expression by suramin treatment. This effect was significantly enhanced when suramin was combined with hyperoxia. Furthermore, pAkt levels decreased following suramin exposure, indicating interference with neurotrophin-dependent growth factor signaling. These data indicate that suramin causes apoptotic cell death and aggravates hyperoxia-induced cell death in immature OLs. Its mechanism of action includes an increase of previously described hyperoxia-induced expression of pro-apoptotic factors and deprivation of growth factor dependent signaling components.

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Section: Discussioncontrasting

confidence: 99%

Section: Suramin Induces and Enhances Apoptosis In A Modelmentioning

confidence: 95%

Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

et al. 2008

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“…The nuclei of the ganglion cells of the treated 19 days old albino rats show peripheral condensation of the chromatin with increase in the granularity of the chromatin as compared with the control. This comes in agreement with Isaev, et al, 1996;Bezvenyuk et al, 2000;and Esrefoglu, et al, 2003. They reported that glutamate excito-toxicity is associated with extensive chromatin condensation.…”

Section: The Ganglion Cell Layersupporting

confidence: 90%

Effect of Monosodium Glutamate on the Post-Natal Development of the Retina of Albino Rat

Saleh

Abd-Elhakim

Mohamad

et al. 2005

Assiut Veterinary Medical Journal

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“…Mitochondrial membrane potential collapses, nuclei swell, and intracellular debris scatter in the incubation medium [19]. Excitotoxicity induced by glutamate is associated with an extensive chromatin condensation and nuclear fragmentation [29]. Excitotoxicity induced by glutamate is associated with an extensive chromatin condensation and nuclear fragmentation [29].…”

Section: Discussionmentioning

confidence: 99%

“…When the mitochondria break down releasing toxic chemicals into cytoplasm, these toxins poison the cell causing destruction of other cell structures including nucleus [28]. Excitotoxicity induced by glutamate is associated with an extensive chromatin condensation and nuclear fragmentation [29]. Isaev et al [23] have shown that acute glutamate toxicity predominantly induces necrotic changes.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural clues for glutamate‐induced necrosis in parietal and cerebellar neurons

Eşrefoğlu

Gepdíremen

Kuruş

2003

Fundamemntal Clinical Pharma

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Glutamate excitotoxicity has been postulated to underlie the neuronal death that occurs after ischemia. The most sensitive tissues to ischemic injury are hippocampus and cerebellum, whereas cerebrum is more resistant. We studied the glutamate-induced ultrastructural alterations in rat parietal and cerebellar neurons comparatively. We observed that glutamate (45 min, 10-7 m) causes considerable nuclear, mitochondrial and cytoplasmic changes in both the neuron types. Mitochondrial and nuclear changes were particularly more severe in cerebellar granular, than the ones in parietal neurons. It has been concluded that glutamate induces necrotic changes in both parietal and cerebellar neurons. But cerebellar cortex was found to be more sensitive to glutamate excitotoxicity than cerebral cortex. We suggest that mitochondrial damage is, probably, an important factor in neuron necrosis, which is mediated by glutamate excitotoxicity.

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Protective effect of suramin against cell death in rat cerebellar granular neurons and mouse neuroblastoma cells

Cited by 7 publications

References 21 publications

Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

Effect of Monosodium Glutamate on the Post-Natal Development of the Retina of Albino Rat

Ultrastructural clues for glutamate‐induced necrosis in parietal and cerebellar neurons

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