Characterization of oxygen-resistant Chinese hamster ovary cells. III. Relative resistance of succinate and α-ketoglutarate dehydrogenases to hyperoxic inactivation

Schoonen, W.G.E.J.; Wanamarta, A.Handayani; Moorsel, J. M. van der Klei-van; Jakobs, Cornelis; Joenje, Hans

doi:10.1016/0891-5849(91)90004-m

Cited by 20 publications

(19 citation statements)

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“…Hyperoxia Induces Growth Arrest at the G 0 /G 1 Phase of the Cell Cycle-Hyperoxia has been reported to induce cell cycle arrest and apoptosis or necrosis (1)(2)(3)(4)(5)(6)(7)32). To determine whether hyperoxia induced adhesion-dependent cell cycle arrest, we performed flow cytometry with DNA staining by propidium iodide.…”

Section: Resultsmentioning

confidence: 99%

“…It has been reported that hyperoxia inhibits cell proliferation and induces cell death in A549 epithelial cells (2, 6), MLE15 murine type II epithelial cells (3), HCT116 colon carcinoma cells (4), Mv1Lu pulmonary adenocarcinoma cells (5,6) and HeLa cells (7). However, few studies have examined the effect of hyperoxia on cell cycle and survival in macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperoxia causes damage to DNA, lipids, and proteins leading to cell cycle arrest and subsequent cell death (1)(2)(3)(4)(5)(6)(7). Hyperoxia-induced growth arrest has been evaluated in epithelial cells (2)(3)(4)(5)(6) and endothelial cells (8,9); however, little is known regarding the effects of hyperoxia on macrophages.…”

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confidence: 99%

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Hyperoxia Induces Macrophage Cell Cycle Arrest by Adhesion-dependent Induction of p21Cip1 and Activation of the Retinoblastoma Protein

Nyunoya

Powers

Yarovinsky

et al. 2003

Journal of Biological Chemistry

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Hyperoxia induces growth arrest, apoptosis, necrosis, and morphological changes (spreading and adhesion) in various types of cells. The mechanism of hyperoxia-induced cell growth arrest has not been well elucidated, especially in macrophages. One possible mechanism is a role of cell adhesion in hyperoxia-induced cell cycle arrest. To evaluate this finding, macrophages were cultured in normoxia (21% O 2 ) or hyperoxia (95% O 2 ) in adhesion or low adhesion conditions. Incubation of macrophages in hyperoxia induced cell cycle arrest. The hyperoxia-induced cell cycle arrest was prevented by low adhesion conditions. To evaluate pathways potentially involved in hyperoxia-induced growth arrest, we measured extracellular regulated kinase and retinoblastoma protein activation and p21Cip1 and p53 accumulation. Hyperoxia strongly induced activation of extracellular regulated kinase and retinoblastoma protein as well as up-regulation of p21Cip1 . These effects of hyperoxia were attenuated under low adhesion conditions, suggesting a role for integrin-dependent signaling. The induction of p21 Cip1 and activation of retinoblastoma protein occurred via a p53-independent mechanism. These results suggest that adhesiondependent pathways are required for hyperoxia-induced cell cycle arrest in macrophages.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hyperoxia Induces Macrophage Cell Cycle Arrest by Adhesion-dependent Induction of p21Cip1 and Activation of the Retinoblastoma Protein

Nyunoya

Powers

Yarovinsky

et al. 2003

Journal of Biological Chemistry

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“…Oxidative stress can also lead to cell death (24). For example, exposure of Hela or CHO cells to 80% O 2 for 2 days inhibits cell growth and leads to loss of reproductive capacity (25)(26). In CHO cells, loss of cell growth correlates with total inhibition of KGDHC (26).…”

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confidence: 99%

“…For example, exposure of Hela or CHO cells to 80% O 2 for 2 days inhibits cell growth and leads to loss of reproductive capacity (25)(26). In CHO cells, loss of cell growth correlates with total inhibition of KGDHC (26). H 2 O 2 also reduces KGDHC activity in intact cardiac mitochondria (27), synaptosomes (28), fibroblasts (29) and N2a cells (30).…”

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confidence: 99%

Reduction in the E2k Subunit of the α-Ketoglutarate Dehydrogenase Complex Has Effects Independent of Complex Activity

Shi

Chen

et al. 2005

Journal of Biological Chemistry

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The activity of the ␣-ketoglutarate dehydrogenase complex (KGDHC) declines in brains of patients with several neurodegenerative diseases. KGDHC consists of multiple copies of E1k, E2k, and E3. E1k and E2k are unique to KGDHC and may have functions independent of the complex. The present study tested the consequences of different levels of diminished E2k mRNA on protein levels of the subunits, KGDHC activity, and physiological responses. Human embryonic kidney cells were stably transfected with an E2k sense or antisense expression vector. Sense control (E2k-mRNA-100) was compared with two clones in which the mRNA was reduced to 67% of control (E2k-mRNA-67) or to 30% of control (E2k-mRNA-30). The levels of the E2k protein in clones paralleled the reduction in mRNA, and E3 proteins were unaltered. Unexpectedly, the clone with the greatest reduction in E2k protein (E2k-mRNA-30) had a 40% increase in E1k protein. The activity of the complex was only 52% of normal in E2k-mRNA-67 clone, but was near normal (90%) in E2k-mRNA-30 clone. Subsequent experiments tested whether the physiological consequences of a reduction in E2k mRNA correlated more closely to E2k protein or to KGDHC activity. Growth rate, increased DCF-detectable reactive oxygen species, and cell death in response to added oxidant were proportional to E2k proteins, but not complex activity. These results were not predicted because subunits unique to KGDHC have never been manipulated in mammalian cells. These results suggest that in addition to its essential role in metabolism, the E2k component of KGDHC may have other novel roles.

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Pathways to Oxidative Cell Death

Horowitz

1998

Acute Respiratory Distress Syndrome

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Characterization of oxygen-resistant Chinese hamster ovary cells. III. Relative resistance of succinate and α-ketoglutarate dehydrogenases to hyperoxic inactivation

Cited by 20 publications

References 19 publications

Hyperoxia Induces Macrophage Cell Cycle Arrest by Adhesion-dependent Induction of p21Cip1 and Activation of the Retinoblastoma Protein

Hyperoxia Induces Macrophage Cell Cycle Arrest by Adhesion-dependent Induction of p21Cip1 and Activation of the Retinoblastoma Protein

Reduction in the E2k Subunit of the α-Ketoglutarate Dehydrogenase Complex Has Effects Independent of Complex Activity

Pathways to Oxidative Cell Death

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