Use of Proteomics to Demonstrate a Hierarchical Oxidative Stress Response to Diesel Exhaust Particle Chemicals in a Macrophage Cell Line

ABSTRACT Serum glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) activity is reduced over 75% in systemic inflammatory response syndrome. To investigate the mechanism of this response, expression of the GPI-PLD gene was studied in the mouse monocyte-macrophage cell line RAW 264.7 stimulated with lipopolysaccharide (LPS; 0.5 to 50 ng/ml). GPI-PLD mRNA was reduced approximately 60% in a time- and dose-dependent manner. Oxidative stress induced by 0.5 mM H2O2 or 50 μM menadione also caused a greater than 50% reduction in GPI-PLD mRNA. The antioxidant N-acetyl-l-cysteine attenuated the down-regulatory effect of H2O2but not of LPS. Cotreatment of the cells with actinomycin D inhibited down-regulation induced by either LPS or H2O2. The half-life of GPI-PLD mRNA was not affected by LPS, or decreased slightly with H2O2, indicating that the reduction in GPI-PLD mRNA is due primarily to transcriptional regulation. Stimulation with tumor necrosis factor alpha (TNF-α) resulted in ∼40% reduction in GPI-PLD mRNA in human A549 alveolar carcinoma cells but not RAW 264.7 cells, suggesting that alternative pathways could exist in different cell types for down-regulating GPI-PLD expression during an inflammatory response and the TNF-α autocrine signaling mechanism alone is not sufficient to recapitulate the LPS-induced reduction of GPI-PLD in macrophages. Sublines of RAW 264.7 cells with reduced GPI-PLD expression exhibited increased cell sensitivity to LPS stimulation and membrane-anchored CD14 expression on the cell surface. Our data suggest that down-regulation of GPI-PLD could play an important role in the control of proinflammatory responses.

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Induction of oxidative stress and TNF-α secretion by Dichloroacetonitrile, a water disinfectant by-product, as possible mediators of apoptosis or necrosis in a murine macrophage cell line (RAW)

Toxicology in Vitro ◽

10.1016/s0887-2333(00)00019-9 ◽

2000 ◽

Vol 14 (3) ◽

pp. 199-210 ◽

Cited By ~ 18

Author(s):

A.E. Ahmed ◽

J. Aronson ◽

S. Jacob

Keyword(s):

Oxidative Stress ◽

Cell Line ◽

Murine Macrophage ◽

Macrophage Cell Line ◽

Macrophage Cell ◽

Murine Macrophage Cell Line ◽

Tnf Α

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PCB congener specific oxidative stress response by microarray analysis using human liver cell line

Environment International ◽

10.1016/j.envint.2010.05.011 ◽

2010 ◽

Vol 36 (8) ◽

pp. 907-917 ◽

Cited By ~ 29

Author(s):

Supriyo De ◽

Somiranjan Ghosh ◽

Raghunath Chatterjee ◽

Y-Q Chen ◽

Linda Moses ◽

...

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Cell Line ◽

Microarray Analysis ◽

Liver Cell ◽

Human Liver ◽

Oxidative Stress Response ◽

Liver Cell Line ◽

Human Liver Cell

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High Fructose Negatively Impacts Proliferation of NSC-34 Motor Neuron Cell Line

Journal of Neurosciences in Rural Practice ◽

10.1055/s-0041-1742120 ◽

2022 ◽

Author(s):

Divya Lodha ◽

Jamuna R. Subramaniam

Keyword(s):

Oxidative Stress ◽

Stress Response ◽

Motor Neuron ◽

Cell Line ◽

Motor Neurons ◽

Response Regulator ◽

Oxidative Stress Response ◽

Ros Generation ◽

Multinucleated Cells ◽

High Fructose

Abstract Objectives The main aim of this study is to identify the deleterious effects of indiscriminately consumed high fructose on motor neurons that are critically affected in many neurological conditions causing movement disorders including paralysis. Materials and Methods Neuroblastoma x mouse spinal cord motor neuron cell line (NSC-34) motor neuron cell lines were treated with high fructose and oxygen supplementation (18.8%) and assayed for cell proliferation/death, reactive oxygen species (ROS) generation, and oxidative stress response induction Statistical Analysis Mean and standard deviation, significance with and without high fructose (F)-5%, were estimated by t-tests using GraphPad Prism ver. 8.2.1 Results F-5% along with O2 (18.8%) annihilates the cells (∼85%) by day10 and inhibits cell division as observed by the presence of multinucleated cells. Unexpectedly, 1 to 2% of cells that survived, differentiated and displayed progressive neurite extension. Though not healthy, they were viable up to 80 days. F-5% increased ROS levels (∼34%) not accompanied by concomitant enhanced expression of oxidative stress response regulator, the transcription factor, nrf-2, or downstream effector, sod-1. Conclusion High fructose is extremely harmful to NSC-34 motor neuron cell line.

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