Modulation of Glutathione Synthetic Enzymes by Acidic Fibroblast Growth Factor

Choi, Jinah; Opalenik, Susan R.; Wu, Wei-Cheng; Thompson, John A.; Forman, Henry Jay

doi:10.1006/abbi.1999.1677

Cited by 12 publications

(4 citation statements)

References 52 publications

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“…Other observations suggested that mitochondrial energy deprivation is concomitant with, or the result of, mitochondrial oxidative stress in AIDS (for example, from HIV itself) or from NRTI therapy with its mitochondrial effects. In vivo studies with NRTI treatment of inbred mice [29,35] support this latter part of the hypothesis and data from our group and others employing transgenic mice revealed that oxidative stress results from transgenic expression of HIV Tat in the heart or liver [36][37][38]. The above-mentioned processes may result from oxidative mtDNA damage, aberrant mtDNA replication and/or altered mtRNA transcription.…”

Section: Mitochondrial Dna Replication Defectssupporting

confidence: 74%

Nucleoside Reverse Transcriptase Inhibitors, Mitochondrial Dna and Aids Therapy

Lewis

2005

Antiviral Therapy

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Section: Mitochondrial Dna Replication Defectssupporting

confidence: 74%

Nucleoside Reverse Transcriptase Inhibitors, Mitochondrial Dna and Aids Therapy

Lewis

2005

Antiviral Therapy

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“…And γ-GC is an intermediate which is produced by γ-glutamyl-cysteine synthetase (GCS) from the amino acid substrates glutamate and cysteine [27]. As described in the E2 protein, Se can accelerate the amino acid substrates cysteine increase, so the activities of GCS could be stimulated subsequently.…”

Section: Discussionmentioning

confidence: 99%

Differential protein expression of Caco-2 cells treated with selenium nanoparticles compared with sodium selenite and selenomethionine

Yan

Ruan

et al. 2014

Nanoscale Res Lett

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The study was designed to determine the differential protein expression of Caco-2 cells treated with different forms of selenium including sodium selenite, selenomethionine (Se-Met), and selenium nanoparticles (nano-Se). Two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and mass spectrometry (MS) were used to identify the differentially expressed proteins. The results indicated that seven protein spots, ubiquitin-conjugating enzyme E2 (E2), glutathione synthetases (GS), triosephosphate isomerase (TSP), T-complex protein 1 subunit zeta (TCPZ), lamin-B1, heterogeneous nuclear ribonucleoprotein F (hnRNP F), and superoxide dismutase [Cu-Zn] (Cu, Zn-SOD) were significantly different among all the groups. According to the order of control, sodium selenite, Se-Met, and Nano-Se, the expression levels of two proteins (E2 and GS) increased and the other differential proteins were reverse. Except for E2, there were no significant differences in other protein expressions between the groups treated with nano-Se and Se-Met.

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“…Extracellular acid fibroblast growth factor (FGF-1) has been demonstrated to cause transformation and aggressive cell growth in murine embryonic fibroblasts. Recent data from CHOI et al [100] have shown that expression of a chimeric human FGF-1 gene containing a signal peptide sequence for secretion (hst/ KS0FGF-1) in an embryonic fibroblast cell line caused increased gene expression of both c-GCS subunits associated with increased c-GCS activity without elevation of intracellular GSH levels [100]. They suggested that an increase in GSH content per se is not required for altered cell growth though increased expression of c-GCS and c-GCS activity is associated with a common response to growth factors.…”

Section: Effect Of Growth Factorsmentioning

confidence: 99%

Oxidative stress and regulation of glutathione in lung inflammation

Rahman¹,

MacNee²

2000

Eur Respir J

808

555

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Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance, a major cause of cell damage. The development of an oxidant/antioxidant imbalance in lung inflammation may activate redox‐sensitive transcription factors such as nuclear factor‐κB, and activator protein‐1 (AP‐1), which regulate the genes for pro‐inflammatory mediators and protective antioxidant genes. Glutathione (GSH), a ubiquitous tripeptide thiol, is a vital intra‐ and extracellular protective antioxidant against oxidative/nitrosative stresses, which plays a key role in the control of pro‐inflammatory processes in the lungs. Recent findings have suggested that GSH is important in immune modulation, remodelling of the extracellular matrix, apoptosis and mitochondrial respiration. The rate‐limiting enzyme in GSH synthesis is γ‐glutamylcysteine synthetase (γ‐GCS). The human γ‐GCS heavy and light subunits are regulated by AP‐1 and antioxidant response elements and are modulated by oxidants, phenolic antioxidants, growth factors, and inflammatory and anti‐inflammatory agents in lung cells. Alterations in alveolar and lung GSH metabolism are widely recognized as a central feature of many inflammatory lung diseases such as idiopathic pulmonary fibrosis, acute respiratory distress syndrome, cystic fibrosis and asthma. The imbalance and/or genetic variation in antioxidant γ‐GCS and pro‐inflammatory versus antioxidant genes in response to oxidative stress and inflammation in some individuals may render them more susceptible to lung inflammation. Knowledge of the mechanisms of GSH regulation and balance between the release and expression of pro‐ and anti‐inflammatory mediators could lead to the development of novel therapies based on the pharmacological manipulation of the production as well as gene transfer of this important antioxidant in lung inflammation and injury. This review describes the redox control and involvement of nuclear factor‐κB and activator protein‐1 in the regulation of cellular glutathione and γ‐glutamylcysteine synthetase under conditions of oxidative stress and inflammation, the role of glutathione in oxidant‐mediated susceptibility/tolerance, γ‐glutamylcysteine synthetase genetic susceptibility and the potential therapeutic role of glutathione and its precursors in protecting against lung oxidant stress, inflammation and injury.

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Modulation of Glutathione Synthetic Enzymes by Acidic Fibroblast Growth Factor

Cited by 12 publications

References 52 publications

Nucleoside Reverse Transcriptase Inhibitors, Mitochondrial Dna and Aids Therapy

Nucleoside Reverse Transcriptase Inhibitors, Mitochondrial Dna and Aids Therapy

Differential protein expression of Caco-2 cells treated with selenium nanoparticles compared with sodium selenite and selenomethionine

Oxidative stress and regulation of glutathione in lung inflammation

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