Regulation of the Synthesis and Secretion of Plasminogen Activators by Endothelial Cells

Hinsbergh, Victor W.M. van

doi:10.1159/000215814

Cited by 60 publications

(44 citation statements)

References 102 publications

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“…5) We have already confirmed the presence of some fibrinolytic enzymes, plasminogen, plasmin (EC 3.4.21.7)-like activity and two types of plasminogen activators, urokinase (EC 3.4.21.73) and t-PA, in rabbit arteries; however, no thrombin (EC 3.4.21.5)-like enzymes were released from rabbit arteries by treatment with chondroitin sulfate. 1,3) Furthermore, the enhancement of AA activities produced by dermatan sulfate (chondroitin sulfate B; DS) depends on the endothelium, whereas spontaneous AA activities do not depend on the endothelium.…”

Section: 4)supporting

confidence: 54%

Effect of Chondroitinase on Dermatan Sulfate-Facilitated Arginine Amidase Released from Rabbit Ear Artery

Ishii-Nozawa

Naito

Mita

et al. 2010

Biological & Pharmaceutical Bulletin

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We have previously reported that trypsin (EC 3.4.21.4)-like enzymes, showing lysine and arginine p-nitroanilidederivative hydrolyzing activities (arginine amidase activity, AA activity), which can be separated using aprotinin and lima bean inhibitor affinity columns, are secreted from rabbit arteries.1,2) Moreover, we showed that AA released from isolated rabbit ear arteries was accelerated by the addition of mucopolysaccharide sulfate derivatives; heparin, chondroitin sulfate, dextran sulfate and dermatan sulfate.

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Section: 4)supporting

confidence: 54%

Effect of Chondroitinase on Dermatan Sulfate-Facilitated Arginine Amidase Released from Rabbit Ear Artery

Ishii-Nozawa

Naito

Mita

et al. 2010

Biological & Pharmaceutical Bulletin

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“…As a selective barrier between the blood and the surrounding tissues, intact endothelium mechanically separates platelets and their pro-coagulant products from intravascular, subendothelial and tissue coagulation factors, and it also inhibits pro-coagulant proteins (Eisenberg 1991). It controls the passage of materials and the transit of white blood cells into and out of the bloodstream, reduces turbulence of the flow of blood, allows the fluid to be pumped further and participates in fibrinolysis by the production of tissue plasminogen activator (tPA) (Van Hinsbergh 1988). There are also highly differentiated endothelial cells which perform specialized "filtering" functions.…”

Section: The Endotheliummentioning

confidence: 99%

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Bauer¹,

Sotníková²

2010

gpb

134

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Abstract. Vascular endothelium plays a key role in the local regulation of vascular tone and vascular architecture by release of vasodilator and vasoconstrictor substances, as well as factors with pro-coagulant, anticoagulant, fibrinolytic, antibacterial properties, growth factors, chemokines, free radicals, etc. Release of endothelium-derived relaxing factors such as nitric oxide (NO), prostaglandins and endothelium-derived hyperpolarizing factor, as well as vasoconstricting factors such as endothelin, superoxide and thromboxanes play an influential role in the maintenance and regulation of vascular tone and the corresponding peripheral vascular resistance. Under physiological conditions, the release of anticoagulant and smooth muscle relaxing factors exceeds the release of other substances. The first part of this review presents the functions of the endothelium itself, the nature of the endothelium-derived relaxing factor, its production by NO synthases, mechanisms of its action via activation of soluble guanylyl cyclase and production of cyclic 3'-5'-guanosine monophosphate. The resulting biological effects include vasodilatation, regulation of vessel wall structure, increased regional blood perfusion, lowering of systemic blood pressure, antithrombosis and antiatherosclerosis effects, which counteract the vascular actions of endogenous vasoconstrictor substances. Impaired endothelial function, either as a consequence of reduced production/release or increased inactivation of endothelium-derived vasodilators, as well as interactions of NO with angiotensin, reactive oxygen species and oxidized lipoproteins, has detrimental functional consequences and is one of the most important cardiovascular risk factors. Therefore the second part of this review assesses the pathophysiologic impact of the endothelium in examples of cardiovascular pathologies, e.g. endotheliopathies caused by increased angiotensin production, lipid peroxidation, ischemia/reperfusion or diabetes.

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“…The cellular basis of endogenous fibrinolysis has been the subject of numerous speculations and investigations. Endothelial cells are a major source of tPA and PAIs (37)(38)(39)(40). Activated macrophages and smooth muscle cells are another source of PAs and PAIs (41)(42)(43)(44).…”

Section: Ast Cells Are Multifunctional Effector Cells That Partic-mentioning

confidence: 99%

Production of Plasminogen Activator Inhibitor-1 by Human Mast Cells and Its Possible Role in Asthma

Cho¹,

Tam²,

Demissie-Sanders³

et al. 2000

The Journal of Immunology

118

114

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The plasminogen activator inhibitor type 1 (PAI-1) has an essential role in tissue remodeling. The PAI-1 gene was induced by a combination of phorbol ester and calcium ionophore at the highest level among the inducible human mast cell genes that we have analyzed on a DNA microarray. PAI-1 was secreted by both a human mast cell line (HMC)-1 and primary cultured human mast cells upon stimulation, whereas PAI-1 was undetectable in either group of unstimulated cells. The secretion of PAI-1 was due to de novo synthesis of PAI-1 rather than secretion of preformed PAI-1. The functional significance of PAI-1 secretion was demonstrated by complete inhibition of tissue-type plasminogen activator activity with supernatants of stimulated HMC-1 cells. Furthermore, we were able to regulate PAI-1 gene expression in HMC-1 cells by known therapeutic agents. High-dose (1 μM) dexamethasone induced PAI-1 mRNA expression. Cyclosporin down-regulated the expression of the PAI-1 gene. Cycloheximide abrogated PAI-1 mRNA expression, suggesting that transcription of the PAI-1 gene requires de novo synthesis of early gene products, including transcription factors. Finally, we demonstrated PAI-1 in lung mast cells from a patient with asthmatic attack by double-immunofluorescence study. This is the first report demonstrating that activated human mast cells release a striking amount of functionally active PAI-1. These results suggest that PAI-1 could play an important role in airway remodeling of asthma, and inhibition of PAI-1 activity could represent a novel therapeutic approach in the management of airway remodeling.

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Regulation of the Synthesis and Secretion of Plasminogen Activators by Endothelial Cells

Cited by 60 publications

References 102 publications

Effect of Chondroitinase on Dermatan Sulfate-Facilitated Arginine Amidase Released from Rabbit Ear Artery

Effect of Chondroitinase on Dermatan Sulfate-Facilitated Arginine Amidase Released from Rabbit Ear Artery

Nitric oxide – the endothelium-derived relaxing factor and its role in endothelial functions

Production of Plasminogen Activator Inhibitor-1 by Human Mast Cells and Its Possible Role in Asthma

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