Vascular smooth muscle cell effect on endothelial cell endothelin-1 production

Luozzo, Gabriele Di; Bhargava, Jaya; Powell, Richard J.

doi:10.1067/mva.2000.103788

Cited by 38 publications

(20 citation statements)

References 26 publications

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“…2,13,16,20 Studies in arterial intimal hyperplasia following vascular injury have demonstrated that SMC inhibit EC secretion of endothelin (ET-1), a potent SMC mitogen, by increasing the activity of eNOS and increasing NO concentration in the EC/SMC microenvironment. 9 In modules seeded with HUVEC (with or without UVSMC), the secretion of NO decreased over time (14 days). This may be due to the proliferation 5 and migration of seeded HUVEC over the time span.…”

Section: Effect Of Embedded Uvsmc On Huvec Phenotypementioning

confidence: 99%

“…31 Using the same co-culture system, this group also demonstrated that endothelin-1 (ET-1) secretion by EC was inhibited by SMC through its modulation of endothelial nitric oxide synthase (eNOS) activity. 9 On the other hand, an increase in eNOS activity inhibits SMC proliferation and prevents hyperplasia. 18 In both conditioned medium and a transwell system 10 proliferating EC have been shown to enhance the growth of SMC.…”

Section: Introductionmentioning

confidence: 99%

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A Modular Tissue Engineering Construct Containing Smooth Muscle Cells and Endothelial Cells

Leung

Sefton

2007

Ann Biomed Eng

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Human umbilical vein endothelial cells (HUVEC) were seeded on sub-mm sized collagen cylinders containing embedded umbilical vein smooth muscle cells (UVSMC). These cylindrical "modules" are intended to be used as a vascularized construct, in which HUVEC lined channels are created by the random packing of the modules in situ or within a larger container. Embedding UVSMC cultured in medium containing 10% FBS had an adverse effect on subsequently seeded HUVEC junction morphology; HUVEC/UVSMC co-culturing was done in HUVEC medium (2% FBS with the addition of 0.03 mg/mL endothelial cell growth supplement) as compared to HUVEC seeded on collagen-only modules. In contrast, embedding UVSMC cultured in serum-free medium prior to embedding improved EC junction morphology. Such serum-free culturing, also prevented the UVSMC induced contraction of the collagen modules. On the other hand, embedding serum-free cultured UVSMC promoted HUVEC proliferation and NO secretion compared to those modules embedded with 10% serum cultured UVSMC. These results suggest, not surprisingly, that embedded UVSMC phenotype plays an important role in the seeded HUVEC phenotype, and that the response can be modulated by the UVSMC culture medium serum concentration. These studies were undertaken with a view to using the UVSMC to modulate the thrombogenicity of the HUVEC. Exploration of this outcome awaits further studies directed to understanding the mechanism of the cellular interactions.

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Section: Effect Of Embedded Uvsmc On Huvec Phenotypementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Modular Tissue Engineering Construct Containing Smooth Muscle Cells and Endothelial Cells

Leung

Sefton

2007

Ann Biomed Eng

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“…These data are not surprising, because endothelin-1 is not able to inhibit basal nitric oxide production, whereas nitric oxide can inhibit endothelin-1 activity on internal mammary arteries and decrease endothelin-1 production in smooth muscle cell. This effect seems mediated through endothelin-B receptor activity [17,40,57].…”

Section: Similarities and Differences Between Cardiac Andmentioning

confidence: 99%

Role of Endothelial Dysfunction and Insulin Resistance in Angina Pectoris and Normal Coronary Angiogram

Monti

Piatti²

2005

Herz

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Angina pectoris and a normal coronary angiogram or cardiac syndrome X is a heterogeneous syndrome that probably encompasses different pathophysiological entities. Patients affected by cardiac syndrome X are often women presenting with severe, invalidating chest pain. However, there is a significant discrepancy among the severity of symptoms, the lack of hemodynamic evidence of myocardial ischemia and the relatively benign long-term prognosis. The vascular endothelium has numerous important functions, including the regulation of vascular tone, blood flow and permeability, secreting both vasorelaxing and vasoconstricting factors. It has been found that both endothelium and non-endothelium-mediated coronary blood flow are impaired in patients with cardiac syndrome X. Interestingly, it has been shown that impaired nitric oxide-dependent vasodilation could increase coronary microvessel tone and produce spasm. It has also been reported that circulating endothelin-1 levels are elevated with a direct relationship between endothelin-1 levels and impaired coronary flow reserve in these patients. In addition, patients with high endothelin-1 levels showed a time onset of chest pain during exercise significantly lower compared to patients with low endothelin-1 concentrations. Moreover, the nitric oxide/endothelin-1 ratio was found decreased in patients with cardiac syndrome X and endothelin-1 levels were also positively correlated with fasting asymmetric dimethylarginine levels. All in all, these data suggest a role of endothelial dysfunction as a cause of regional myocardial and peripheral blood flow abnormalities. Further studies are necessary to characterize the prevailing mechanisms determining alterations in nitric oxide/endothelin-1 pathway in these patients, in order to find new therapies able to improve both quality of life and prognosis.

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“…These data are not surprising, because endothelin-1 is not able to inhibit basal NOx production, 34 whereas NO can inhibit the vasoconstrictive effects of endothelin-1 on internal mammary arteries 35 and decrease endothelin-1 production in smooth muscle cells. 36 In addition, basal NO production can modulate endothelin-1 activity through endothelial endothelin-B receptor activity. 37 Influence of L-Arginine on Insulin-Stimulated Endothelial Function L-Arginine infusion induced important changes in insulininduced NOx, cGMP and endothelin-1 release in patients with CSX.…”

Section: Piatti Et Al L-arginine In Cardiac Syndrome X 433mentioning

confidence: 99%

Acute Intravenous l -Arginine Infusion Decreases Endothelin-1 Levels and Improves Endothelial Function in Patients With Angina Pectoris and Normal Coronary Arteriograms

et al. 2003

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Background-We tested the hypothesis that asymmetric dimethylarginine (ADMA) levels could be elevated and influence endothelin-1 and nitric oxide release and action in patients with cardiac syndrome X (CSX). In addition, we evaluated whether an intravenous infusion of L-arginine would improve endothelial function in these subjects. Methods and Results-Nine patients with CSX and 14 control subjects underwent a continuous infusion of L-arginine (0.125 g/min) or saline for 120 minutes. Sixty minutes after L-arginine or saline infusions, an intravenous insulin bolus (0.1 U/kg) combined with a euglycemic clamp was performed. Basal ADMA and endothelin-1 levels were higher in patients with CSX than in controls. At the end of the first hour of infusion, compared with saline, L-arginine infusion increased basal forearm blood flow, nitrite and nitrate (NOx), and forearm cGMP release and decreased endothelin-1. After insulin bolus, during saline, insulin-induced NOx, endothelin-1, and forearm cGMP release was almost abolished. Conversely, L-arginine restored a physiological profile of all endothelial variables compared with control subjects. In control subjects, compared with saline infusion, L-arginine infusion did not modify any parameter. ADMA levels were positively correlated with basal endothelin-1 levels and negatively correlated with insulin-induced incremental levels of NOx and forearm cGMP release. Conclusions-Plasma ADMA levels are increased in patients with CSX, and they are correlated with increases in endothelin-1 and reductions in insulin-induced increments in plasma NOx and cGMP, effects that are reversed by intravenous L-arginine. These data suggest that increased ADMA levels play a role in the abnormal vascular reactivity that is observed in patients with CSX.

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Vascular smooth muscle cell effect on endothelial cell endothelin-1 production

Cited by 38 publications

References 26 publications

A Modular Tissue Engineering Construct Containing Smooth Muscle Cells and Endothelial Cells

A Modular Tissue Engineering Construct Containing Smooth Muscle Cells and Endothelial Cells

Role of Endothelial Dysfunction and Insulin Resistance in Angina Pectoris and Normal Coronary Angiogram

Acute Intravenous l -Arginine Infusion Decreases Endothelin-1 Levels and Improves Endothelial Function in Patients With Angina Pectoris and Normal Coronary Arteriograms

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