Expression and distribution of redox regulatory protein, thioredoxin during transient focal brain ischemia in the rat

Takagi, Yasushi; Horikawa, Fumihiko; Nozaki, Kazuhiko; Sugino, Toshiyuki; Hashimoto, Nobuo; Yodoi, Junji

doi:10.1016/s0304-3940(98)00492-3

Cited by 48 publications

(23 citation statements)

References 18 publications

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“…Trx [Trx-(SH) 2 ] also provides the electrons for the reduction of peroxides, which is catalyzed by peroxiredoxins (Prx). [76][77][78]. Immunohistochemical analysis of Trx1 in human brain [79] showed positive Trx1-like staining in white matter astrocytes.…”

Section: Basal Expression Of Trxs In the Cnsmentioning

confidence: 95%

“…A growing number of studies report a striking association between Trx1 up-regulation in the CNS during neuron survival following various injuries resulting in oxidative stress (see table1). Mechanical nerve injury and transient focal brain ischemia induce Trx1 in various brain areas and cell types, with induction patterns suggesting Trx1 function(s) in neuroprotection or regeneration of the brain following injury and oxidative stress [74][75][76][77][78]81]. Neuronal survival was associated with Trx1 up-regulation in response to ischemic stress [77,78,82].…”

Section: Trx Induction In the Cnsmentioning

confidence: 99%

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Emerging roles of thioredoxin cycle enzymes in the central nervous system

Patenaude¹,

Murthy

Mirault

2005

CMLS, Cell. Mol. Life Sci.

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The thioredoxins (Trxs) constitute a family of enzymes which catalyze the reduction of protein disulfide bonds. Recent animal studies have revealed the importance of the Trx superfamily in various experimental systems. For example, the homozygous disruption of the genes encoding cytoplasmic (TRX1) or mitochondrial Trx (TRX2) in mice generates lethal embryonic phenotypes. In contrast, transgenic mice overexpressing TRX1 show an extended life span and are relatively resistant to ischemia- mediated brain damage. In addition to their capacity to detoxify peroxides in concert with peroxiredoxins and Trx reductases, Trx isozymes perform multiple redox signaling functions mediated by their specific interaction with various proteins, including redox-regulated kinases and transcription factors. Recent studies indicate that specific isoforms of Trx cycle enzymes, targeted to different cell compartments, are key regulators of fundamental processes, such as gene expression, cell growth and apoptosis. The present review is primarily focused on the emerging neuroprotective role of these proteins in the central nervous system.

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Section: Basal Expression Of Trxs In the Cnsmentioning

confidence: 95%

Section: Trx Induction In the Cnsmentioning

confidence: 99%

Emerging roles of thioredoxin cycle enzymes in the central nervous system

Patenaude¹,

Murthy

Mirault

2005

CMLS, Cell. Mol. Life Sci.

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“…Counter-staining was not performed. The immunohistochemistric examination was performed 3 to 4 times and the reactivity of TRX and 8-OHdG semiquantitatively determined on a scale of mild, moderate, and severe according to the method of Takagi et al 8,[15][16][17] The most frequently scored reactivity was considered to be representative for the lesions.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Miyamoto¹,

Kishimoto²,

Shioji³

et al. 2001

Jpn Circ J

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“…Specific sub-mitochondrial localization to the inner mitochondrial membrane and high resistance to oxidation suggest that Trx-2 provides a primary line of defense against ROS, which is generated during mitochondrial respiratory chain functioning. 46) In addition, Trx-2 has documented anti-apoptotic action, in particular, based on the prevention of cytochrome c release from the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Oxidized Peroxiredoxin-3 in Cadmium- and Ceramide-induced Apoptosis of Human Neuroblastoma Cells

Chae

Ahn

et al. 2009

JOURNAL OF HEALTH SCIENCE

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Cadmium (Cd) is an environmental pollutant that produces numerous toxic effects in humans. Previous reports have demonstrated that Cd induces neurodegeneration and other diseases. To study the mechanism of Cd-induced neurodegeneration, SH-SY5Y cells were exposed to Cd. Cd-induced ceramide production was observed in the cells in a time-and dose-dependent manner. Ceramide is a well known lipid second messenger. Previous reports have shown that accumulation of ceramide, triggered by oxidative stress or anticancer drugs, induces apoptosis. To identify proteins involved in cellular responses to Cd or ceramide, we performed comparative proteome analysis using high-resolution two-dimensional gel electrophoresis (2-DE). Four different proteins were identified by combination of mass spectrometry and peptide fingerprinting. Among them, the level of oxidized peroxiredoxin-3 (Prx-3) simultaneously increased in Cd-and ceramide-exposed cells. Furthermore, we observed Cd-or ceramide-induced generation of reactive oxygen species (ROS), leading to SH-SY5Y cell apoptosis. Pretreatment with Trolox helped scavenge Cd-or ceramide-induced ROS and prevented apoptosis, suggesting that Cd-or ceramide-induced cell death can be attributed to ROS production. Here, we elucidate the link between Cd-induced apoptosis and ROS scavenger system in SH-SY5Y cells.

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Expression and distribution of redox regulatory protein, thioredoxin during transient focal brain ischemia in the rat

Cited by 48 publications

References 18 publications

Emerging roles of thioredoxin cycle enzymes in the central nervous system

Emerging roles of thioredoxin cycle enzymes in the central nervous system

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice

Involvement of Oxidized Peroxiredoxin-3 in Cadmium- and Ceramide-induced Apoptosis of Human Neuroblastoma Cells

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