scholarly journals Low glucose induces mitochondrial reactive oxygen species via fatty acid oxidation in bovine aortic endothelial cells

2017 ◽  
Vol 8 (6) ◽  
pp. 750-761 ◽  
Author(s):  
Nobuhiro Kajihara ◽  
Daisuke Kukidome ◽  
Kiminori Sada ◽  
Hiroyuki Motoshima ◽  
Noboru Furukawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Low Glucose

Oxidized phospholipids mediate occludin expression and phosphorylation in vascular endothelial cells

2006 ◽  
Vol 290 (2) ◽  
pp. H674-H683 ◽  
Author(s):  
Lucas DeMaio ◽  
Mahsa Rouhanizadeh ◽  
Srinivasa Reddy ◽  
Alex Sevanian ◽  
Juliana Hwang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Reactive Oxygen ◽  
Diffusive Flux ◽  
Oxygen Species ◽  
Aortic Endothelial Cells ◽  
Zonula Occludens ◽  
Bovine Aortic Endothelial Cells ◽  
Zonula Occludens 1 ◽  
Aortic Endothelial

Oxidized l-α-1-palmitoyl-2-arachidonoyl- sn-glycero-3-phosphorylcholine (OxPAPC), a component of minimally modified LDL, induces production of proinflammatory cytokines and development of atherosclerotic lesions. We tested the hypothesis that OxPAPC alters expression, phosphorylation, and localization of tight junction (TJ) proteins, particularly occludin, a transmembrane TJ protein. OxPAPC reduced total occludin protein and increased occludin phosphorylation dose dependently (10–50 μg/ml) and time dependently in bovine aortic endothelial cells. OxPAPC decreased occludin mRNA and reduced the immunoreactivity of zonula occludens-1 at the cell-cell contacts. Furthermore, OxPAPC increased the diffusive flux of 10-kDa dextran in a dose-dependent manner. O2−· production by bovine aortic endothelial cells increased nearly twofold after exposure to OxPAPC. Also, enzymatic generation of O2−· by xanthine oxidase-lumazine and H2O2 by glucose oxidase-glucose increased occludin phosphorylation, implicating reactive oxygen species as modulators of the OxPAPC effects on occludin phosphorylation. Superoxide dismutase and/or catalase blocked the effects of OxPAPC on occludin protein content and phosphorylation, occludin mRNA, zonula occludens-1 immunoreactivity, and diffusive flux of 10-kDa dextran. These findings suggest that changes in TJ proteins are potential mechanisms by which OxPAPC compromises the barrier properties of the vascular endothelium. OxPAPC-induced disruption of TJs, which likely facilitates transmigration of LDL and inflammatory cells into the subendothelial layers, may be mediated by reactive oxygen species.

Role of xanthine oxidoreductase and NAD(P)H oxidase in endothelial superoxide production in response to oscillatory shear stress

2003 ◽  
Vol 285 (6) ◽  
pp. H2290-H2297 ◽  
Author(s):  
J. Scott McNally ◽  
Michael E. Davis ◽  
Don P. Giddens ◽  
Aniket Saha ◽  
Jinah Hwang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Oscillatory Shear ◽  
Oxygen Species ◽  
Aortic Endothelial Cells ◽  
Protein Levels ◽  
Text Production ◽  
Bovine Aortic Endothelial Cells ◽  
Oscillatory Shear Stress

Oscillatory shear stress occurs at sites of the circulation that are vulnerable to atherosclerosis. Because oxidative stress contributes to atherosclerosis, we sought to determine whether oscillatory shear stress increases endothelial production of reactive oxygen species and to define the enzymes responsible for this phenomenon. Bovine aortic endothelial cells were exposed to static, laminar (15 dyn/cm2), and oscillatory shear stress (±15 dyn/cm2). Oscillatory shear increased superoxide ([Formula: see text]) production by more than threefold over static and laminar conditions as detected using electron spin resonance (ESR). This increase in [Formula: see text] was inhibited by oxypurinol and culture of endothelial cells with tungsten but not by inhibitors of other enzymatic sources. Oxypurinol also prevented H2O2 production in response to oscillatory shear stress as measured by dichlorofluorescin diacetate and Amplex Red fluorescence. Xanthine-dependent [Formula: see text] production was increased in homogenates of endothelial cells exposed to oscillatory shear stress. This was associated with decreased xanthine dehydrogenase (XDH) protein levels and enzymatic activity resulting in an elevated ratio of xanthine oxidase (XO) to XDH. We also studied endothelial cells lacking the p47 phox subunit of the NAD(P)H oxidase. These cells exhibited dramatically depressed [Formula: see text] production and had minimal XO protein and activity. Transfection of these cells with p47 phox restored XO protein levels. Finally, in bovine aortic endothelial cells, prolonged inhibition of the NAD(P)H oxidase with apocynin decreased XO protein levels and prevented endothelial cell stimulation of [Formula: see text] production in response to oscillatory shear stress. These data suggest that the NAD(P)H oxidase maintains endothelial cell XO levels and that XO is responsible for increased reactive oxygen species production in response to oscillatory shear stress.

scholarly journals Lineage-Selective Disturbance of Early Human Hematopoietic Progenitor Cell Differentiation by the Commonly Used Plasticizer Di-2-ethylhexyl Phthalate via Reactive Oxygen Species: Fatty Acid Oxidation Makes the Difference

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2703
Author(s):  
Lars Kaiser ◽  
Isabel Quint ◽  
René Csuk ◽  
Manfred Jung ◽  
Hans-Peter Deigner
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Energy Production ◽  
Hematopoietic Cells ◽  
Reactive Oxygen ◽  
Health Concern ◽  
Acid Oxidation ◽  
Oxygen Species ◽  
Ethylhexyl Phthalate

Exposure to ubiquitous endocrine-disrupting chemicals (EDCs) is a major public health concern. We analyzed the physiological impact of the EDC, di-2-ethylhexyl phthalate (DEHP), and found that its metabolite, mono-2-ethylhexyl phthalate (MEHP), had significant adverse effects on myeloid hematopoiesis at environmentally relevant concentrations. An analysis of the underlying mechanism revealed that MEHP promotes increases in reactive oxygen species (ROS) by reducing the activity of superoxide dismutase in all lineages, possibly via its actions at the aryl hydrocarbon receptor. This leads to a metabolic shift away from glycolysis toward the pentose phosphate pathway and ultimately results in the death of hematopoietic cells that rely on glycolysis for energy production. By contrast, cells that utilize fatty acid oxidation for energy production are not susceptible to this outcome due to their capacity to uncouple ATP production. These responses were also detected in non-hematopoietic cells exposed to alternate inducers of ROS.

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