Cu/Zn superoxide dismutase expression in the postnatal rat brain following an excitotoxic injury

Peluffo, Hugo; Acarín, Laia; Faiz, Maryam; Castellano, Bernardo; González, Berta

doi:10.1186/1742-2094-2-12

Cited by 38 publications

(9 citation statements)

References 67 publications

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“…However, the decrease in neuronal SOD2 that we have noticed at 10 dpi was accompanied by significant up-regulation in highly reactive astroglial cells. A comparable extensive induction in reactive astrocytes and in the astroglial scar was showed for Cu/Zn SOD at 3, 5, and 7 days following excitotoxic injury in the postnatal rat brain (44). Consequently, astrocytes seem to be the main cell type that increases the total antioxidant capabilities in the nervous tissue after a lesion.…”

Section: Discussionsupporting

confidence: 53%

“…Consequently, astrocytes seem to be the main cell type that increases the total antioxidant capabilities in the nervous tissue after a lesion. The fact that they are more capable of handling oxidative stress conditions can explain their elevated resistance to cell death after an injury (44). In this regard, previous studies showed that Cu/Zn SOD-overexpressing astrocytes had increased resistance to oxidative damage (45).…”

Section: Discussionmentioning

confidence: 99%

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Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats

et al. 2012

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AimTo evaluate the effect of hyperbaric oxygen therapy (HBOT) on superoxide dismutase 2 (SOD2) expression pattern after the cortical stab injury (CSI).MethodsCSI was performed on 88 male Wistar rats, divided into control, sham, lesioned, and HBO groups. HBOT protocol was the following: pressure applied was 2.5 absolute atmospheres, for 60 minutes, once a day for consecutive 3 or 10 days.‎ The pattern of SOD2 expression and cellular localization was analyzed using real-time polymerase chain reaction, Western blot, and double-label fluorescence immunohistochemistry. Neurons undergoing degeneration were visualized with Fluoro-Jade®B.ResultsCSI induced significant transient increase in SOD2 protein levels at day 3 post injury, which was followed by a reduction toward control levels at post-injury day 10. At the same time points, mRNA levels for SOD2 in the injured cortex were down-regulated. Exposure to HBO for 3 days considerably down-regulated SOD2 protein levels in the injured cortex, while after 10 days of HBOT an up-regulation of SOD2 was observed. HBOT significantly increased mRNA levels for SOD2 at both time points compared to the corresponding L group, but they were still lower than in controls. Double immunofluorescence staining revealed that 3 days after CSI, up-regulation of SOD2 was mostly due to an increased expression in reactive astrocytes surrounding the lesion site. HBOT attenuated SOD2 expression both in neuronal and astroglial cells. Fluoro-Jade®B labeling showed that HBOT significantly decreased the number of degenerating neurons in the injured cortex.ConclusionHBOT alters SOD2 protein and mRNA levels after brain injury in a time-dependent manner.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats

et al. 2012

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“…Tomato lectin has been widely used as a marker of microglia/macrophages and endothelial cells in the CNS [ 55 , 56 ]. Here, we show that tomato lectin is also a good marker for macrophages in the normal and lesioned nerve when compared to Iba-1 and F4/80 (Figs.…”

Section: Resultsmentioning

confidence: 99%

CD300f immunoreceptor contributes to peripheral nerve regeneration by the modulation of macrophage inflammatory phenotype

Peluffo

Solari-Saquieres

Negro-Demontel

et al. 2015

J Neuroinflammation

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BackgroundIt has recently become evident that activating/inhibitory cell surface immune receptors play a critical role in regulating immune and inflammatory processes in the central nervous system (CNS). The immunoreceptor CD300f expressed on monocytes, neutrophils, and mast cells modulates inflammation, phagocytosis, and outcome in models of autoimmune demyelination, allergy, and systemic lupus erythematosus. On the other hand, a finely regulated inflammatory response is essential to induce regeneration after injury to peripheral nerves since hematogenous macrophages, together with resident macrophages and de-differentiated Schwann cells, phagocyte distal axonal and myelin debris in a well-orchestrated inflammatory response. The possible roles and expression of CD300f and its ligands have not been reported under these conditions.MethodsBy using quantitative PCR (QPCR) and CD300f-IgG2a fusion protein, we show the expression of CD300f and its ligands in the normal and crush injured sciatic nerve. The putative role of CD300f in peripheral nerve regeneration was analyzed by blocking receptor-ligand interaction with the same CD300f-IgG2a soluble receptor fusion protein in sciatic nerves of Thy1-YFP-H mice injected at the time of injury. Macrophage M1/M2 polarization phenotype was also analyzed by CD206 and iNOS expression.ResultsWe found an upregulation of CD300f mRNA and protein expression after injury. Moreover, the ligands are present in restricted membrane patches of Schwann cells, which remain stable after the lesion. The lesioned sciatic nerves of Thy1-YFP-H mice injected with a single dose of CD300f-IgG2a show long lasting effects on nerve regeneration characterized by a lower number of YFP-positive fibres growing into the tibial nerve after 10 days post lesion (dpl) and a delayed functional recovery when compared to PBS- or IgG2a-administered control groups. Animals treated with CD300f-IgG2a show at 10 dpl higher numbers of macrophages and CD206-positive cells and lower levels of iNOS expression than both control groups. At later time points (28 dpl), increased numbers of macrophages and iNOS expression occur.ConclusionsTaken together, these results show that the pair CD300f ligand is implicated in Wallerian degeneration and nerve regeneration by modulating both the influx and phenotype of macrophages.

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“…Here, we show that tanshinone IIA was able to reduce ROS level and MDA and protein carbonyl contents and also enhance activities and expressions of the antioxidant enzymes SOD and CAT in glutamate-exposed SH-SY5Y cells (Table 1), demonstrating its antioxidant capacity. Intriguingly, a number of antioxidant enzymes are known to have distinct isoforms, for example, cytoplasmic Cu/ZnSOD, mitochondrial MnSOD, and extracellular Cu/ZnSOD are the three SOD isoforms in mammalian cells, and it has been demonstrated that excessive excitatory amino acids can reduce the activities and expressions of SOD isoforms [39, 40]. On the other hand, decreased SOD activity and expression are shown to increase excitotoxicity in experimental models [41, 42], while increased enzymatic activity and protein level of SOD isoforms are reported to alleviate excitotoxicity [42, 43].…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Han

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Glutamate excitotoxicity is associated with many neurological diseases, including cerebral ischemia and neurodegenerative diseases. Tanshinone IIA, a diterpenoid naphthoquinone from Salvia miltiorrhiza, has been shown to suppress presynaptic glutamate release, but its protective mechanism against glutamate-induced neurotoxicity is lacking. Using SH-SY5Y human neuroblastoma cells, we show here that excessive glutamate exposure decreases cell viability and proliferation and increases LDH release. Pretreatment with tanshinone IIA, however, prevents the decrease in cell viability and proliferation and the increase in LDH release induced by glutamate. Tanshinone IIA also attenuates glutamate-induced oxidative stress by reducing reactive oxygen species level and malondialdehyde and protein carbonyl contents and by enhancing activities and protein levels of superoxide dismutase and catalase. We then show that tanshinone IIA prevents glutamate-induced mitochondrial dysfunction by increasing mitochondrial membrane potential and ATP content and by reducing mitochondrial protein carbonyl content. Moreover, tanshinone IIA can inhibit glutamate-induced apoptosis through regulation of apoptosis-related protein expression and MAPK activation, including elevation of Bcl-2 protein level, decrease in Bax and cleaved caspase-3 levels, and suppression of JNK and p38 MAPK activation. Collectively, our findings demonstrate that tanshinone IIA protects SH-SY5Y cells against glutamate toxicity by reducing oxidative stress and regulating apoptosis and MAPK pathways.

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Cu/Zn superoxide dismutase expression in the postnatal rat brain following an excitotoxic injury

Cited by 38 publications

References 67 publications

Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats

Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats

CD300f immunoreceptor contributes to peripheral nerve regeneration by the modulation of macrophage inflammatory phenotype

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

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