Correlation between thrombin-induced prostacyclin production and inositol trisphosphate and cytosolic free calcium levels in cultured human endothelial cells.

Jaffe, Eric; Grulich, J; Weksler, Babette B.; Hampel, G; Watanabe, Kentaro

doi:10.1016/s0021-9258(18)47450-9

Cited by 273 publications

(18 citation statements)

References 60 publications

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“…For instance, arterial bifurcations and bends frequently exhibit flow detachment and the formation of recirculation zones (Malek et al 1999), resulting in a spatially varying chemical concentration along the vessel wall. Physiologically important biochemical factors known to interact with the artery wall via endothelial cell (EC) receptormediated reactions include (but are not restricted to) adenosine nucleotides, thrombin, histamine and bradykinin (Jaffe et al 1987;Tran et al 2000;Yamamoto et al 2000). In addition, blood-borne macromolecules such as lipoproteins are transported from the bloodstream to the arterial intima via trans-endothelial filtration (Phelps & DePaola 2000;Stangeby & Ethier 2002).…”

Section: Introductionmentioning

confidence: 99%

Concentration of blood-borne agonists at the endothelium

et al. 2005

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The delivery of endothelial ligands and macromolecules, such as lipoproteins, from the circulation to the arterial wall is of central importance in modulating endothelial cell function and physiology and, consequently, in the onset of vascular disease. Given the strong spatial correlation between areas of disturbed blood flow and occurrence of atherosclerotic plaque, a detailed understanding of the effects of different fluid flow characteristics on the delivery of factors in the bloodstream to the endothelium is an essential step towards understanding the observed localization of vascular disease to certain focal sites within the vasculature. In this paper, a model of biochemical mass transport in a two-dimensional flow chamber with spatially varying wall shear stress is presented. The advantage of the relatively simple arterial geometry is that all the essential features of blood flow in vivo are captured, but the underlying effects on mass transport, and, hence, on endothelial cell function, are not masked by complex three-dimensional flow. Indeed, it is demonstrated that a previously derived similarity solution, in terms of the shear stress on the endothelial wall, is an asymptotically close approximation to the exact solution to the advection–diffusion equation. The mathematical analysis is then used to identify fundamental links between the wall shear stress and the distribution of chemical species along the endothelium. The physiological implications of these links are discussed, in particular the location of maximum chemical concentration on the endothelium, which is of great significance to the regulation of intracellular signalling and, consequently, endothelial cell function.

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Section: Introductionmentioning

confidence: 99%

Concentration of blood-borne agonists at the endothelium

et al. 2005

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“…Extensive in vivo studies have characterized thrombin to be a potent activator of the vascular barrier causing vasoconstriction (Horgan et al 1987), endothelial leakiness (Malik and Horgan, 1987) and pulmonary accumu-Journal of Cell Science 96, 737-744 (1990) Printed in Great Britain ©The Company of Biologists Limited 1990 lation of leukocytes (Cooper et al 1984). In vitro, thrombin leads to endothelial synthesis of various biologically active products (Jaffe et al 1987;Weksler et al 1978;Galdal et al 1985;Levin et al 1984;Prescott et al 1984) and is responsible for enhanced endothelial permeability probably caused by endothelial gap formation (Laposata et al 1983). In addition, human thrombin was described as eliciting a short-time effect on neutrophil adherence to human umbilical vein endothelial cells (HUVE) (Zimmerman et al 1986) and it was also reported that thrombin induces adherence of neutrophils to endothelial cells following a long preincubation in a homologous ovine system (Bizios et al 1988).…”

Section: Introductionmentioning

confidence: 99%

Promotion of transendothelial neutrophil passage by human thrombin

Moser

Groscurth

Fehr

1990

Journal of Cell Science

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Thrombin has been reported to elicit two temporally different effects on neutrophil-endothelial interaction, categorically described as ‘neutrophil adhesion’: one expressed within a few minutes, the other after several hours of endothelial preincubation. Prolonged activation resulted in often elongated, tightly interacting neutrophils in contact with human umbilical vein endothelial cells (HUVE) mainly at the intercellular region. In contrast, the neutrophil-endothelial interaction due to short-time priming with thrombin was dominated by round, randomly distributed neutrophils, loosely adhering on the endothelial surface. Sheer stress, introduced to characterize these morphological entities in a quantitative manner, clearly defined the neutrophil response due to short time priming as sheer stresslabile compared to the sheer stress-resistant interaction expressed after prolonged preincubation of HUVE with thrombin. Quantitative determination of neutrophil transendothelial migration served to demonstrate the relevance of such differences in neutrophil binding with respect to subsequent layer penetration. Dependent upon endothelial protein synthesis and inhibited by antithrombin-III-heparin and hirudin, neutrophil layer penetration only occurred after prolonged activation of HUVE whereas the neutrophil-endothelial interaction due to short time priming with thrombin was limited to superficial neutrophil adhesion. We conclude that thrombin can be added to the list of activators capable of inducing the neutrophil passage-guiding principle, an effect that has recently been detected as closely related to neutrophil adhesion to endothelial ligands expressed upon activation with interleukin-1 and tumor necrosis factor. This biological activity, which can be separated from superficial attachment of polymorphonuclear leukocytes (PMN) to endothelial cells, is a catalytic site-dependent and late phase-specific effect of thrombin on HUVE.

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“…Αυτός είναι πιθανότατα και ο μόνος πρακτικά εφαρμόσιμος τρόπος για την invivo αναστολή της δράσης της θρομβίνης, αφού δεν υπάρχει σε ευρεία χρήση κάποιος άλλος γνωστός παράγοντας που να διακόπτει την ενεργοποίηση του υποδοχέα της θρομβίνης. [326] Επιπρόσθετα, η πιθανότητα ύπαρξης [130,[132][133][134][135] διαφόρων υποτύπων υποδοχέων της θρομβίνης περιπλέκει ακόμη περισσότερο την προσπάθεια φαρμακευτικής αναστολής της δράσης της και η δέσμευση των αιμοπεταλιακού τύπου υποδοχέων της πιθανότατα να μην είναι αρκετή σε περιπτώσεις κυτταρικών στόχων που διαθέτουν διαφόρους υποδοχείς που ενεργοποιούνται μετά από σύνδεση με αυτή.…”

Section: αιματική ροή νεφρικού φλοιούunclassified

“…Τέλος, πρέπει να αναφερθεί το ότι από μελέτες invitro έχει φανεί ότι σε κυτταρικές καλλιέργειες, τα επιθηλιακά κύτταρα του αγγειώδους σπειράματος και τα μεσαγγειακά κύτταρα παρουσιάζουν ανταπόκριση στην θρομβίνη, με πολλαπλασιασμό και με σύνθεση και παραγωγή προσταγλανδινών, νιτρικού οξειδίου, ενδοθηλίνης-1, στοιχείων του εξωκυτταρίου υποστρώματος, και χημειοκινών όπως η χημειοτακτική πρωτεΐνη των μονοκυττάρων ή MCP-1.Έχοντας υπόψιν τους μηχανισμούς δράσης της θρομβίνης, συνυπολογίζοντας και το δεδομένο της αύξησης των επιπέδων και της ενεργότητάς της κατά την επαναιμάτωση, μπορεί να υποστηριχθεί ότι η αναστολή της, μέσω χορήγησης Αντιθρομβίνης ΙΙΙ, θα ήταν πιθανό να μειώνει τις βλάβες κατά το σύνδρομο ισχαιμίας και επαναιμάτωσης. Πράγματι, υπάρχουν πειραματικά δεδομένα, που υποστηρίζουν την προστατευτική ιδιότητα της αντιθρομβίνης, μέσω της αναστολής της δράσης της θρομβίνης [129][130][131][132][133][134]. …”

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Η Αντιθρομβίνη ΙΙΙ Στην Πρόληψη Της Νεφρικής Βλάβης Μετά Από Εντερική Ισχαιμία Και Σύνδρομο Επαναιμάτωσης

Τσάχαλης¹,

Tsachalis²

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Correlation between thrombin-induced prostacyclin production and inositol trisphosphate and cytosolic free calcium levels in cultured human endothelial cells.

Cited by 273 publications

References 60 publications

Concentration of blood-borne agonists at the endothelium

Concentration of blood-borne agonists at the endothelium

Promotion of transendothelial neutrophil passage by human thrombin

Η Αντιθρομβίνη ΙΙΙ Στην Πρόληψη Της Νεφρικής Βλάβης Μετά Από Εντερική Ισχαιμία Και Σύνδρομο Επαναιμάτωσης

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