Eicosanoid Metabolism and Endothelial Cell Adhesion Molecule Expression: Effects on Platelet/Vessel Wall Interactions

Buchanan, Michael R.; Bertomeu, Maria C.; Brister, Stephanie J.; Haas, Thomas A.

doi:10.1007/978-1-4615-3754-0_17

Cited by 5 publications

(5 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The CD fat source is soybean oil, which provides 9.14g/kg of PUFAs while the WD, with milk fat provides 7.35g/kg (a decrease in n-3 PUFAS from 1.21 to 1.05 g/kg and n-6 PUFA’s from 7.93 to 6.3). Interestingly, in LDLr -/- mice, we saw an increase in the long chain (20 and 22 carbon) neuroprotective PUFAs [ 101 ], and a decrease in 9-Hydroxy-10,12-octadecadienoic acid (9-HODE), a pro-inflammatory mediator [ 102 ] and 13-HODE, shown to regulate platelet vessel wall adhesion [ 103 , 104 ], and commonly associated with a protective effect. This may be due to a shift in the types or quantities of lipids normally delivered across the BBB [ 81 ].…”

Section: Discussionmentioning

confidence: 99%

Reduced cognitive function, increased blood-brain-barrier transport and inflammatory responses, and altered brain metabolites in LDLr -/-and C57BL/6 mice fed a western diet

et al. 2018

View full text Add to dashboard Cite

Recent work suggests that diet affects brain metabolism thereby impacting cognitive function. Our objective was to determine if a western diet altered brain metabolism, increased blood-brain barrier (BBB) transport and inflammation, and induced cognitive impairment in C57BL/6 (WT) mice and low-density lipoprotein receptor null (LDLr -/-) mice, a model of hyperlipidemia and cognitive decline. We show that a western diet and LDLr -/- moderately influence cognitive processes as assessed by Y-maze and radial arm water maze. Also, western diet significantly increased BBB transport, as well as microvessel factor VIII in LDLr -/- and microglia IBA1 staining in WT, both indicators of activation and neuroinflammation. Interestingly, LDLr -/- mice had a significant increase in 18F- fluorodeoxyglucose uptake irrespective of diet and brain 1H-magnetic resonance spectroscopy showed increased lactate and lipid moieties. Metabolic assessments of whole mouse brain by GC/MS and LC/MS/MS showed that a western diet altered brain TCA cycle and β-oxidation intermediates, levels of amino acids, and complex lipid levels and elevated proinflammatory lipid mediators. Our study reveals that the western diet has multiple impacts on brain metabolism, physiology, and altered cognitive function that likely manifest via multiple cellular pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Reduced cognitive function, increased blood-brain-barrier transport and inflammatory responses, and altered brain metabolites in LDLr -/-and C57BL/6 mice fed a western diet

et al. 2018

View full text Add to dashboard Cite

show abstract

“…NO and prostacyclin, which inhibit platelet adhesion and aggregation, are constitutively released by endothelial cells (223). 3-hydroxyoctadecadienoic acid, synthesized via lipoxygenase pathways in resting endothelial cells, inhibit platelet aggregation by acting as a negative regulator for the adhesion receptor vitronectin (35, 36). Membrane-bound ectonucleotidases on cell surface of endothelial cells metabolize ATP and ADP to prevent platelet activation (191, 289).…”

Section: Functions Of the Endotheliummentioning

confidence: 99%

Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling

Thakore

Earley

2019

Comprehensive Physiology

View full text Add to dashboard Cite

The vascular endothelium is a broadly distributed and highly specialized organ. The endothelium has a number of functions including the control of blood vessels diameter through the production and release of potent vasoactive substances or direct electrical communication with underlying smooth muscle cells, regulates the permeability of the vascular barrier, stimulates the formation of new blood vessels, and influences inflammatory and thrombotic processes. Endothelial cells that make up the endothelium express a variety of cell-surface receptors and ion channels on the plasma membrane that are capable of detecting circulating hormones, neurotransmitters, oxygen tension, and shear stress across the vascular wall. Changes in these stimuli activate signaling cascades that initiate an appropriate physiological response. Increases in the global intracellular Ca 2+ concentration and localized Ca 2+ signals that occur within specialized subcellular microdomains are fundamentally important components of many signaling pathways in the endothelium. The transient receptor potential (TRP) channels are a superfamily of cationpermeable ion channels that act as a primary means of increasing cytosolic Ca 2+ in endothelial cells. Consequently, TRP channels are vitally important for the major functions of the endothelium. In this review, we provide an in-depth discussion of Ca 2+-permeable TRP channels in the endothelium and their role in vascular regulation.

show abstract

“…Interestingly, exposure of endothelial cells to HPODE can have beneficial effects. For example, the hydroxyderivative of HPODE, HODE inhibits platelet aggregation (36,37) and production of thromboxane (38). In addition, HPODE has been shown to stimulate prostacyclin synthesis by the endothelium, which may have antiatherogenic effects (39).…”

Section: Discussionmentioning

confidence: 99%

Regulation of endothelial nitric oxide synthase gene expression by oxidized linoleic acid

Ramasamy

Parthasarathy

Harrison

1998

Journal of Lipid Research

View full text Add to dashboard Cite

Hypercholesterolemia is associated with impairments in endothelium-dependent vascular relaxations. Paradoxically, endothelial production of nitrogen oxides is increased in early stages of hypercholesterolemia. Prior work has shown that oxidized low density lipoprotein (LDL) has both stimulatory and inhibitory effects on endothelial nitric oxide synthase expression (eNOS) and has focused on lysophosphatidyl choline (LPC) as a component of oxidized LDL which may modulate this effect. Another biologically active component of oxidized LDL is 13-hydroperoxyoctadecadienoic acid (13-HPODE), an oxidized form of linoleic acid. The purpose of this study was to determine the effect of HPODE on the expression of eNOS in bovine aortic endothelial cells (BAECs). Twenty four hour treatment of endothelial cells with HPODE caused a dose-dependent increase in eNOS mRNA levels as assessed by Northern analysis. The time response studies show that HPODE treatment significantly increased eNOS mRNA levels at 12 and 24 h. Concomitant with the increase in eNOS mRNA levels, 20 m HPODE treatment significantly increased eNOS protein content and enzyme activity. Nuclear run-on studies indicated that the rate of transcription of eNOS gene was significantly elevated 4 h after HPODE treatment when compared to control cultures. Also, actinomycin D studies demonstrated that the half-life of eNOS mRNA was increased from 6 h to 12 h by HPODE treatment. Thus, HPODE-induced up-regulation of eNOS expression is mediated by both transcriptional and posttranscriptional mechanisms.These observations suggest that endothelial cells may attempt to compensate for oxidative injury by increasing expression of eNOS in early stages of hypercholesterolemia. -Ramasamy, S., S. Parthasarathy, and D. G. Harrison. Regulation of endothelial nitric oxide synthase gene expression by oxidized linoleic acid.

show abstract

Eicosanoid Metabolism and Endothelial Cell Adhesion Molecule Expression: Effects on Platelet/Vessel Wall Interactions

Cited by 5 publications

References 24 publications

Reduced cognitive function, increased blood-brain-barrier transport and inflammatory responses, and altered brain metabolites in LDLr -/-and C57BL/6 mice fed a western diet

Reduced cognitive function, increased blood-brain-barrier transport and inflammatory responses, and altered brain metabolites in LDLr -/-and C57BL/6 mice fed a western diet

Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling

Regulation of endothelial nitric oxide synthase gene expression by oxidized linoleic acid

Contact Info

Product

Resources

About