The influence of chylomicron remnants on endothelial cell function in the isolated perfused rat aorta

Endothelial-cell dysfunction is a critical initiating event in the pathogenesis of atherosclerosis. Although there is evidence to suggest that chylomicron remnants (CMRs), lipoproteins derived from the diet, influence endothelial-cell function to generate a pro-atherogenic phenotype, the mechanisms involved remain undefined. We have examined the effects of CMR-like particles (CMR-LPs) on human endothelial-cell function, focusing on the cyclo-oxygenase (COX) and nitric oxide synthase (NOS) pathways. CMR-LPs strongly enhanced the expression of the inducible cyclo-oxygenase COX-2 and increased prostacyclin synthesis in a biphasic manner. Studies with the COX-2-selective inhibitor NS-398 confirmed the COX-2 dependency of the later increase in prostanoid production. Pre-incubation with CMR-LPs reduced basal and thrombin-stimulated cGMP generation, whereas expression of endothelial NOS was not modified by remnant treatment.

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Depression of endothelium-dependent relaxation by filarial parasite products

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.2.h648 ◽

1990 ◽

Vol 259 (2) ◽

pp. H648-H652 ◽

Cited By ~ 5

Author(s):

L. Kaiser ◽

P. K. Tithof ◽

J. F. Williams

Keyword(s):

Endothelial Cell ◽

Conditioned Medium ◽

Cell Function ◽

Rat Aorta ◽

Biologically Active ◽

Exact Nature ◽

Dialysis Tubing ◽

Endothelial Cell Function ◽

Endothelium Dependent Relaxation

Endothelium-dependent relaxation is depressed in the femoral artery of dogs with heartworm, Dirofilaria immitis, infection. Moreover, in infected dogs, the mechanism of relaxation is different. Because D. immitis is located primarily in the pulmonary circulation, these findings suggested that D. immitis releases biologically active mediators that alter distal endothelium-dependent relaxation. We tested this hypothesis in vitro. Rings of rat aorta were exposed to D. immitis (alone, in 1,000 mol wt or 100 mol wt cutoff dialysis tubing, and bioassay with conditioned medium). D. immitis alone depressed relaxation to acetylcholine, carbachol, and A23187. Nitroglycerin relaxation was not affected. Depression of acetylcholine relaxation was seen with D. immitis alone, in 1,000 mol wt dialysis tubing, and bioassay with conditioned medium. However, acetylcholine relaxation with D. immitis in 100 mol wt dialysis tubing was not different from control. It appears that D. immitis releases a small, stable, biologically active factor that alters endothelium-dependent relaxation. Its exact nature is unknown. The study of endothelial cell behavior in filariasis and modulation of endothelial cell function by filarial factors may provide important clues in understanding the pathogenesis of parasitic diseases.

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Endothelial Cell Function, Including Tissue Factor Expression, Under Flow Conditions

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642664 ◽

1995 ◽

Vol 74 (01) ◽

pp. 123-128 ◽

Cited By ~ 40

Author(s):

Eric F Grabowski ◽

Frances P Lam

Keyword(s):

Endothelial Cell ◽

Tissue Factor ◽

Cell Function ◽

Tissue Factor Expression ◽

Flow Conditions ◽

Endothelial Cell Function ◽

Factor Expression

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Do DPP-4 inhibitors improve endothelial cell function?

10.35841/cardiology.1.1.12-14 ◽

2017 ◽

Vol 01 (01) ◽

Author(s):

Hiroshi Nomoto ◽

Hideaki Miyoshi ◽

Akinobu Nakamura ◽

Tatsuya Atsumi ◽

Naoki Manda ◽

...

Keyword(s):

Endothelial Cell ◽

Cell Function ◽

Endothelial Cell Function

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Estrogen Restores Endothelial Cell Function in an Experimental Model of Vascular Injury

Circulation ◽

10.1161/01.cir.96.5.1624 ◽

1997 ◽

Vol 96 (5) ◽

pp. 1624-1630 ◽

Cited By ~ 60

Author(s):

C. Roger White ◽

Jonathan Shelton ◽

Shi-Juan Chen ◽

Victor Darley-Usmar ◽

Leslie Allen ◽

...

Keyword(s):

Endothelial Cell ◽

Experimental Model ◽

Vascular Injury ◽

Cell Function ◽

Endothelial Cell Function

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Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Journal of Endocrinology ◽

10.1530/joe-16-0340 ◽

2017 ◽

Vol 232 (1) ◽

pp. R27-R44 ◽

Cited By ~ 90

Author(s):

D S Boeldt ◽

I M Bird

Keyword(s):

Endothelial Cell ◽

Endothelial Dysfunction ◽

Cell Function ◽

Endothelial Cell Dysfunction ◽

Hypertensive Disorders Of Pregnancy ◽

Endothelial Cell Function ◽

Vascular Adaptation ◽

Cell Dysfunction ◽

Maternal Adaptation ◽

Flow Through

Maternal vascular adaptation to pregnancy is critically important to expand the capacity for blood flow through the uteroplacental unit to meet the needs of the developing fetus. Failure of the maternal vasculature to properly adapt can result in hypertensive disorders of pregnancy such as preeclampsia (PE). Herein, we review the endocrinology of maternal adaptation to pregnancy and contrast this with that of PE. Our focus is specifically on those hormones that directly influence endothelial cell function and dysfunction, as endothelial cell dysfunction is a hallmark of PE. A variety of growth factors and cytokines are present in normal vascular adaptation to pregnancy. However, they have also been shown to be circulating at abnormal levels in PE pregnancies. Many of these factors promote endothelial dysfunction when present at abnormal levels by acutely inhibiting key Ca2+ signaling events and chronically promoting the breakdown of endothelial cell–cell contacts. Increasingly, our understanding of how the contributions of the placenta, immune cells, and the endothelium itself promote the endocrine milieu of PE is becoming clearer. We then describe in detail how the complex endocrine environment of PE affects endothelial cell function, why this has contributed to the difficulty in fully understanding and treating this disorder, and how a focus on signaling convergence points of many hormones may be a more successful treatment strategy.

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