Differential changes in Cu, Zn and Mn superoxide dismutase activity in developing rat brain and liver

Mariucci, Giuseppina; Ambrosini, Maria Vittoria; Colarieti, Lorenza; Bruschelli, G

doi:10.1007/bf01939957

Cited by 31 publications

(13 citation statements)

References 14 publications

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“…32 MnSOD expression has also been associated to the developing rat brain and liver. 33 However, those studies only show a temporal relationship between differentiation and MnSOD upregulation, demonstrating that this is an early event in the cell differentiation process. By using DNA transfection methods, St Clair and coworkers were the first group to report the direct role of MnSOD in mouse embryo fibroblasts differentiation and also in the differentiation program of fibrosarcoma cells.…”

Section: Discussionmentioning

confidence: 97%

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

Quiros

Sáinz

Hevia

et al. 2009

Intl Journal of Cancer

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Despite improvements in diagnosis of advanced prostate cancer (PCa), treatment is not efficient and 5-year survival is still low. Initially, the less abundant of cell types, neuroendocrine cells (NE), are involved in regulatory process but their physiological role is not fully understood. Among others, an increase in NE cells along with tumor progression has been commonly reported but their role in tumorigenesis or the molecular mechanisms of transdifferentiation is still a matter of debate. We have used human PCa cells (LNCaP) induced to differentiate to NE cells with several stimuli: androgen withdrawal, cyclic AMP or treatment with the antioxidant pineal hormone melatonin. PCa patients' specimens were also analyzed by western blotting and by immunocytochemistry. NE-like LNCaP cells express high levels of mitochondrial superoxide dismutase (MnSOD/SOD2) in addition to NE markers. MnSOD upregulation is mediated by NFjB transcription factor, mainly through p65 translocation into the nuclei. More importantly, overexpression of MnSOD induces the rise of NE-markers in LNCaP cells, showing that MnSOD upregulation might be instrumental for NE differentiation in PCa cells. Furthermore, MnSOD is highly expressed in advanced tumors of patients' when compared with control, nonpathological samples or with low-grade tumors, along with the presence of synaptophysin, a common NE marker. Also, fluorescence immunohistochemical analysis revealed that MnSOD colocalizes with NE markers in most of NE cells observed in PCa specimens. The present findings indicate that MnSOD is essential for NE transdifferentiation and mediates in part the differentiation process, which appears also to be critical in vivo. ' 2009 UICC

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Section: Discussionmentioning

confidence: 97%

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

Quiros

Sáinz

Hevia

et al. 2009

Intl Journal of Cancer

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“…However, the role of MnSOD in fALS pathogenesis remains elusive. MnSOD is expressed in almost all mammalian cells, including neurons, and can be induced under various conditions (10,16,37,50). We recently demonstrated that the molecular pathology of FUS mutation can be recapitulated in cell culture (20) and Drosophila (55) models.…”

Section: Discussionmentioning

confidence: 99%

FUsed in Sarcoma Is a Novel Regulator of Manganese Superoxide Dismutase Gene Transcription

Dhar

Zhang²,

Gál³

et al. 2014

Antioxidants & Redox Signaling

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Aims: FUsed in sarcoma (FUS) is a multifunctional DNA/RNA-binding protein that possesses diverse roles, such as RNA splicing, RNA transport, DNA repair, translation, and transcription. The network of enzymes and processes regulated by FUS is far from being fully described. In this study, we have focused on the mechanisms of FUS-regulated manganese superoxide dismutase (MnSOD) gene transcription. Results: Here we demonstrate that FUS is a component of the transcription complex that regulates the expression of MnSOD. Overexpression of FUS increased MnSOD expression in a dose-dependent manner and knockdown of FUS by siRNA led to the inhibition of MnSOD gene transcription. Reporter analyses, chromatin immunoprecipitation assay, electrophoretic mobility shift assay, affinity chromatography, and surface plasmon resonance analyses revealed the far upstream region of MnSOD promoter as an important target of FUS-mediated MnSOD transcription and confirmed that FUS binds to the MnSOD promoter and interacts with specificity protein 1 (Sp1). Importantly, overexpression of familial amyotropic lateral sclerosis (fALS)-linked R521G mutant FUS resulted in a significantly reduced level of MnSOD expression and activity, which is consistent with the decline in MnSOD activity observed in fibroblasts from fALS patients with the R521G mutation. R521G-mutant FUS abrogates MnSOD promoter-binding activity and interaction with Sp1. Innovation and Conclusion: This study identifies FUS as playing a critical role in MnSOD gene transcription and reveals a previously unrecognized relationship between MnSOD and mutant FUS in fALS. Antioxid. Redox Signal. 20, 1550Signal. 20, -1566

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“…49 In addition, the newborn rat, like the preterm human infant, has low levels of superoxide dismutase. 50 Furthermore, recent studies have shown that excitotoxic injury to immature neurons and oligodendrocytes is mediated in part by loss of cellular antioxidants and free radical injury. 51 -52 In summary, this study showed that 100 mg/kg SC deferoxamine rapidly concentrates in the brain of the 7-day-old rat to levels between 100 and 200 ^mol/L.…”

Section: Discussionmentioning

confidence: 99%

Deferoxamine posttreatment reduces ischemic brain injury in neonatal rats.

Palmer

Roberts

Bero

1994

Stroke

199

102

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Background and Purpose Iron catalyzes the formation of damaging reactive species during cerebral reperfusion. Brain iron concentration is highest at birth, so the brain of the asphyxiated newborn may be at increased risk of iron-dependent injury. We investigated whether the ferric iron chelator deferoxamine could reduce hypoxic-ischemic brain injury in neonatal rats. Because deferoxamine has concentrationdependent activities other than iron chelation, we measured brain deferoxamine levels and calculated deferoxamine pharmacokinetic parameters.Methods We produced hypoxic-ischemic injury to the right cerebral hemisphere of 7-day-old rats by right common carotid artery ligation followed by 2.25 hours of hypoxia in 8% oxygen. At 5 minutes of recovery from hypoxia the rats received 100 mg/kg deferoxamine mesylate or saline subcutaneously. Rats (saline, n=33; deferoxamine, n=38) were killed at 42 hours of recovery to assess early acute edema by measurement of hemispheric water content. Other rats (saline, n=31; deferox-

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Differential changes in Cu, Zn and Mn superoxide dismutase activity in developing rat brain and liver

Cited by 31 publications

References 14 publications

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

FUsed in Sarcoma Is a Novel Regulator of Manganese Superoxide Dismutase Gene Transcription

Deferoxamine posttreatment reduces ischemic brain injury in neonatal rats.

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