Redox‐regulated expression of glycolytic enzymes in resting and proliferating rat thymocytes

Hamm-Künzelmann, Brigitte; Schäfer, Doris; Weigert, Cora; Brand, Karl

doi:10.1016/s0014-5793(97)00029-x

Cited by 21 publications

(15 citation statements)

References 17 publications

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“…PGK1 is oxidized in AD and PD mouse model (59), in MCI brain (9), and in PSP (40). Moreover, PKM2 is oxidized in MCI (9) and in Alzheimer brains (9,40), and a correlation has been observed between levels of oxidation and activity of PKM2 in MCI brain (10), and in a rat hepatoma cellular model (27). In agreement with this observation, we demonstrate here that PKM2 is oxidized and its activity decreased in Abcd1-null mice.…”

supporting

confidence: 87%

Oxidative Damage Compromises Energy Metabolism in the Axonal Degeneration Mouse Model of X-Adrenoleukodystrophy

Galino

Ruíz

Fourcade

et al. 2011

Antioxidants & Redox Signaling

105

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Aims: Chronic metabolic impairment and oxidative stress are associated with the pathogenesis of axonal dysfunction in a growing number of neurodegenerative conditions. To investigate the intertwining of both noxious factors, we have chosen the mouse model of adrenoleukodystrophy (X-ALD), which exhibits axonal degeneration in spinal cords and motor disability. The disease is caused by loss of function of the ABCD1 transporter, involved in the import and degradation of very long-chain fatty acids (VLCFA) in peroxisomes. Oxidative stress due to VLCFA excess appears early in the neurodegenerative cascade. Results: In this study, we demonstrate by redox proteomics that oxidative damage to proteins specifically affects five key enzymes of glycolysis and TCA (Tricarboxylic acid) cycle in spinal cords of Abcd1 -mice and pyruvate kinase in human X-ALD fibroblasts. We also show that NADH and ATP levels are significantly diminished in these samples, together with decrease of pyruvate kinase activities and GSH levels, and increase of NADPH. Innovation: Treating Abcd1 -mice with the antioxidants N-acetylcysteine and a-lipoic acid (LA) prevents protein oxidation; preserves NADH, NADPH, ATP, and GSH levels; and normalizes pyruvate kinase activity, which implies that oxidative stress provoked by VLCFA results in bioenergetic dysfunction, at a presymptomatic stage. Conclusion: Our results provide mechanistic insight into the beneficial effects of antioxidants and enhance the rationale for translation into clinical trials for X-adrenoleukodystrophy. Antioxid. Redox Signal. 15, 2095Signal. 15, -2107

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supporting

confidence: 87%

Oxidative Damage Compromises Energy Metabolism in the Axonal Degeneration Mouse Model of X-Adrenoleukodystrophy

Galino

Ruíz

Fourcade

et al. 2011

Antioxidants & Redox Signaling

105

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“…For example, transcriptional down-regulation of aldolase and other glycolytic enzymes was reported under oxidative stress conditions (35). Further, increased expression of aldolase and enhanced resistance to apoptosis were observed in cancer cell lines with constitutive expression of HIF-1␣ (36).…”

Section: Resultsmentioning

confidence: 99%

Identification of a Protective Role for Protein Phosphatase 1cγ1 against Oxidative Stress-induced Vascular Smooth Muscle Cell Apoptosis

Tchivilev¹,

Madamanchi²,

Vendrov

et al. 2008

Journal of Biological Chemistry

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The development of therapeutic strategies to inhibit reactive oxygen species (ROS)-mediated damage in blood vessels has been limited by a lack of specific targets for intervention. Targeting ROS-mediated events in the vessel wall is of interest, because ROS play important roles throughout atherogenesis. In early atherosclerosis, ROS stimulate vascular smooth muscle cell (VSMC) growth, whereas in late stages of lesion development, ROS induce VSMC apoptosis, causing atherosclerotic plaque instability. To identify putative protective genes against oxidative stress, mouse aortic VSMC were infected with a retroviral human heart cDNA expression library, and apoptosis was induced in virus-infected cells by 2,3-dimethoxy-1,4-naphthoquinone (DMNQ) treatment. A total of 17 different, complete cDNAs were identified from the DMNQ-resistant VSMC clones by PCR amplification and sequencing. The cDNA encoding PP1c␥1 (catalytic subunit of protein phosphatase 1) was present in several independent DMNQ-resistant VSMC clones. DMNQ increased mitochondrial ROS production, caspase-3/7 activity, DNA fragmentation, and decreased mitochondrial transmembrane potential in VSMC while decreasing PP1c␥1 activity and expression. Depletion of PP1c␥1 expression by short hairpin RNA significantly enhanced basal as well as DMNQ-induced VSMC apoptosis. PP1c␥1 overexpression abrogated DMNQ-induced JNK1 activity, p53 Ser 15 phosphorylation, and Bax expression and protected VSMC against DMNQ-induced apoptosis. In addition, PP1c␥1 overexpression attenuated DMNQ-induced caspase-3/7 activation and DNA fragmentation. Inhibition of p53 protein expression using small interfering RNA abrogated DMNQ-induced Bax expression and significantly attenuated VSMC apoptosis. Together, these data indicate that PP1c␥1 overexpression promotes VSMC survival by interfering with JNK1 and p53 phosphorylation cascades involved in apoptosis.Enhanced reactive oxygen species (ROS) 3 generation plays an important role in the proliferation, migration, or apoptosis of vascular smooth muscle cells (VSMC), all of which have been implicated in the pathophysiology of vascular diseases, including atherosclerosis. VSMC proliferation and migration are important in the development of atherosclerotic lesions, and VSMC apoptosis is a histologic hallmark of advanced atherosclerosis (1). Additionally, human VSMC isolated from coronary plaques are more susceptible to apoptosis than VSMC isolated from normal arteries (2). Apoptosis of VSMC in atherosclerotic plaques is accompanied by numerous other events that increase the likelihood of plaque rupture. These include decreases in collagen and extracellular matrix protein production, decreased fibrous cap thickness, accumulation of macrophages along the shoulder of the plaque, and increases in the size of the necrotic core and amount of cellular debris within the plaque (3). A better understanding of the mechanisms that regulate VSMC apoptosis could lead to the development of strategies to stabilize atherosclerotic plaques.Identifying genes that c...

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“…The SP family members are usually associated with basal promoter activity, however, they contain zinc finger sulfhydryl groups that are sensitive to oxidation and direct redox changes alter SP regulated transcription (34,35). Wu et al (35) demonstrated that oxidizing conditions led to a decrease in SP1 binding and promoter activity in HeLa cells.…”

Section: Discussionmentioning

confidence: 99%

“…Wu et al (35) demonstrated that oxidizing conditions led to a decrease in SP1 binding and promoter activity in HeLa cells. This occurred in extracts from cells treated with oxidizing agents and extracts treated directly.…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of Na,K-ATPase β1 Transcription by Hyperoxia Is Mediated by SP1/SP3 Binding

Wendt¹,

Gick²,

Sharma³

et al. 2000

Journal of Biological Chemistry

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The sodium pump, Na,K-ATPase, is an important protein for maintaining intracellular ion concentration, cellular volume, and ion transport and is regulated both transcriptionally and post-transcriptionally. We previously demonstrated that hyperoxia increased Na,KATPase ␤ 1 gene expression in Madin-Darby canine kidney (MDCK) cells. In this study, we identify a DNA element necessary for up-regulation of the Na,K-ATPase ␤ 1 transcription by hyperoxia and evaluate the nuclear proteins responsible for this up-regulation. Transient transfection experiments in MDCK cells using sequential 5-deletions of the rat Na,K-ATPase ␤ 1 promoterluciferase fusion gene demonstrated promoter activation by hyperoxia between ؊102 and ؉151. The hyperoxia response was localized to a 7-base pair region between ؊62 and ؊55, which contained a GC-rich region consistent with a consensus sequence for the SP1 family, that was sufficient for up-regulation by hyperoxia. This GC element exhibited both basal and hyperoxia-induced promoter activity and bound both transcription factors SP1 and SP3 in electrophoretic mobility shift assays. In addition, electrophoretic mobility shift assays demonstrated increased binding of SP1/SP3 in cells exposed to hyperoxia while mutation of this element eliminated protein binding. Other GC sites within the proximal promoter also demonstrated up-regulation of transcription by hyperoxia, however, the site at ؊55 had higher affinity for SP proteins.

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Redox‐regulated expression of glycolytic enzymes in resting and proliferating rat thymocytes

Cited by 21 publications

References 17 publications

Oxidative Damage Compromises Energy Metabolism in the Axonal Degeneration Mouse Model of X-Adrenoleukodystrophy

Oxidative Damage Compromises Energy Metabolism in the Axonal Degeneration Mouse Model of X-Adrenoleukodystrophy

Identification of a Protective Role for Protein Phosphatase 1cγ1 against Oxidative Stress-induced Vascular Smooth Muscle Cell Apoptosis

Up-regulation of Na,K-ATPase β1 Transcription by Hyperoxia Is Mediated by SP1/SP3 Binding

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