The Experts below are selected from a list of 300 Experts worldwide ranked by ideXlab platform
David J. Schneider - One of the best experts on this subject based on the ideXlab platform.
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Intramural Plasminogen Activator Inhibitor Type-1 and Coronary Atherosclerosis
Arteriosclerosis thrombosis and vascular biology, 2003Co-Authors: Burton E. Sobel, Douglas J. Taatjes, David J. SchneiderAbstract:Altered expression of Plasminogen Activator Inhibitor type-1 in vessel walls, reviewed here, might affect coronary atherogenesis. Upregulation might exacerbate vasculopathy by potentiating thrombosis and by inhibiting vascular smooth muscle cell migration, resulting in attenuation of thickness of elaborated fibrous caps implicated in the vulnerability of atheroma to rupture.
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Plasminogen Activator Inhibitor type 1 in adults with Down syndrome and protection against macrovascular disease.
The American journal of cardiology, 2000Co-Authors: William E. Hopkins, Burton E. Sobel, Naomi K. Fukagawa, David J. SchneiderAbstract:In the present study we have shown that adults with Down syndrome have reduced Plasminogen Activator Inhibitor type-1 in blood compared with control subjects matched for age, gender, and body mass. Reduced Plasminogen Activator Inhibitor type-1 may explain the low incidence of atherosclerotic vascular disease and its complications that are attributable to plaque instability, such as myocardial infarction and unstable angina, in subjects with Down syndrome, despite an ever-increasing life expectancy.
Michael E. Boulton - One of the best experts on this subject based on the ideXlab platform.
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Oxygen modulates the release of urokinase and Plasminogen Activator Inhibitor-1 by retinal pigment epithelial cells
The international journal of biochemistry & cell biology, 2001Co-Authors: Jonathan T. Erichsen, J. Jarvis-evans, A. Khaliq, Michael E. BoultonAbstract:The aims of this study were to examine the effect of oxygen, in the presence or absence of exogenous growth factors, on the release of Plasminogen Activators and Plasminogen Activator Inhibitor-1 by cultured human retinal pigment epithelial cells. Antigen and activity levels of urokinase, tissue Plasminogen Activator and Plasminogen Activator Inhibitor were measured in conditioned media after cells were exposed to three different oxygen environments: hypoxia, normoxia and hyperoxia. Overall proteolytic balance was determined by zymography. The effects of exogenous basic fibroblast growth factor and transforming growth factor-beta were also examined. it was found that retinal pigment epithelial cells released urokinase, tissue Plasminogen Activator and Plasminogen Activator Inhibitor in measurable quantities. After 48 h, urokinase levels were highest at normoxia, reaching 7.2ng/106 cells (±2.0 SEM), whereas Plasminogen Activator Inhibitor 1 levels were highest at hyperoxia, reaching 67.5ng/106 cells (±3.7 SEM). Tissue Plasminogen Activator levels were minimal (
Francois Hyafil - One of the best experts on this subject based on the ideXlab platform.
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Urokinase and type I Plasminogen Activator Inhibitor production by normal human hepatocytes : modulation by inflammatory agents
Hepatology, 1994Co-Authors: Nathalie Busso, Edwige Nicodeme, Christophe Chesne, André Guillouzo, Dominique Belin, Francois HyafilAbstract:We examined the effects of inflammatory cytokines (interleukin-1 beta, tumor necrosis factor-alpha and transforming growth factor-beta) on the Plasminogen Activator system (urokinase, tissue-type Plasminogen Activator, type 1 Plasminogen Activator Inhibitor) in primary cultures of human hepatocytes. We show that interleukin-1 beta and tumor necrosis factor-alpha increase urokinase-type Plasminogen Activator production, reinforcing the concept that increased urokinase production is associated with inflammatory processes. By contrast, the same agents (i.e., interleukin-1 beta and tumor necrosis factor-alpha) do not stimulate Plasminogen Activator Inhibitor type 1 production. This latter observation rules out hepatocytes as a major cellular source of plasmatic Plasminogen Activator Inhibitor type 1 during acute-phase-related responses. Among the inflammatory agents used, transforming growth factor-beta was found to be the most effective modulator of both urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor type 1, inducing severalfold increases of activity of urokinase-type Plasminogen Activator, antigen and the corresponding mRNA and increasing Plasminogen Activator Inhibitor type 1 antigen and mRNA levels. Urokinase-type Plasminogen Activator and Plasminogen Activator Inhibitor type 1 modulation by transforming growth factor-beta may play a critical role in hepatic pathophysiology.
Peter Mikus - One of the best experts on this subject based on the ideXlab platform.
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Plasminogen Activator Inhibitor Type-2
Advances in Experimental Medicine and Biology, 1997Co-Authors: Peter MikusAbstract:Plasminogen Activator Inhibitor type-2 (PAI-2) is a quite unusual Serpin. Unlike most other Serpins, which are secreted proteins with well characterized target proteinases and function, PAI-2 exists in both cytosolic and secreted forms; its physiological role is not well understood.
Peter A. Campochiaro - One of the best experts on this subject based on the ideXlab platform.
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Modulation of Plasminogen Activator Inhibitor-1 and urokinase in retinal pigmented epithelial cells
Investigative ophthalmology & visual science, 1993Co-Authors: Sean F. Hackett, Peter A. CampochiaroAbstract:Purpose. To examine the effect of several agents that either stimulate or inhibit neovascularization on Plasminogen Activator Inhibitor-1 and urokinase in retinal pigmented epithelial cells and vascular endothelial cells. Methods. Steady-state levels of messenger RNA were assessed by Northern blots and dot blots and protein levels were assessed by immunoprecipitation. Results. Data indicate that messenger RNA levels for Plasminogen Activator Inhibitor-1 are modulated in similar fashion in both cells types, being increased by incubation with transformatoin growth factor-beta, dexamethasone, tumor necrosis factor, phorbol myristate acetate, and thrombin