A study on the action of vitamin E supplementation on plasminogen activator inhibitor type 1 and platelet nitric oxide production in type 2 diabetic patients

2008 ◽  
Vol 18 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Arianna Vignini ◽  
Laura Nanetti ◽  
Cinzia Moroni ◽  
Roberto Testa ◽  
Cristina Sirolla ◽  
...  
Keyword(s):  
Plasminogen Activator Inhibitor ◽  
Diabetic Patients ◽  
Nitric Oxide Production ◽  
Type 2 Diabetic Patients ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Type 2 Diabetic ◽  
Activator Inhibitor

Differential expression of plasminogen activators and their inhibitors in an organotypic skin coculture system

1993 ◽  
Vol 106 (1) ◽  
pp. 45-53 ◽  
Author(s):  
C.S. Chen ◽  
B. Lyons-Giordano ◽  
G.S. Lazarus ◽  
P.J. Jensen
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Urokinase Plasminogen Activator ◽  
Basal Cells ◽  
Type Plasminogen Activator ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor

Using immunohistochemistry and in situ hybridization, we have characterized the expression and localization of components of the plasminogen activator proteolytic cascade in an organotypic coculture system which consists of a “dermal” portion (human dermal fibroblasts throughout a collagen matrix) and a stratified, well-differentiated epidermal portion. Specifically, the following components were examined: the enzymes urokinase-type plasminogen activator and tissue-type plasminogen activator and their type 1 and type 2 inhibitors. Urokinase plasminogen activator mRNA and antigen were found predominantly in the least differentiated, basal keratinocytes; in some fields there was also faint deposition of antigen beneath the basal cells. The distribution of plasminogen activator inhibitor type 1 was similar to that of urokinase, except that inhibitor type 1 antigen deposition beneath the basal cells appeared more intense and uniform. In contrast to the results with urokinase plasminogen activator and inhibitor type 1, tissue plasminogen activator mRNA and antigen were localized focally in the suprabasal, i.e. more differentiated, keratinocytes. Plasminogen activator inhibitor type 2 mRNA and antigen were detected in most epidermal layers, but were more intense suprabasally and often spared the basal layer. These studies demonstrate that the same type of cell, i.e. the keratinocyte, can express different components of the plasminogen activator cascade depending on its state of differentiation. The change in expression of plasminogen activator cascade components with keratinocyte differentiation suggests distinct epidermal functions for these components, related to cell-matrix interaction and epidermal differentiation.

Increased Plasminogen Activator Inhibitor Activity in Non Insulin Dependent Diabetic Patients – Relationship with Plasma Insulin

1989 ◽  
Vol 61 (03) ◽  
pp. 370-373 ◽  
Author(s):  
I Juhan-Vague ◽  
C Roul ◽  
M C Alessi ◽  
J P Ardissone ◽  
M Heim ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Apolipoprotein B ◽  
Plasma Insulin ◽  
Plasminogen Activator Inhibitor ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic ◽  
Activator Inhibitor ◽  
Normal Controls

SummaryType 2 diabetic patients are known to frequently have a high insulin level and were recently described as having high plasminogen activator inhibitor (PAI) activity, compared to normal controls. As we have shown in several clinical conditions (normal subjects, obese patients, angina pectoris patients) that plasma PAI activity was linked with plasma insulin, we have studied in 38 type 2 diabetic patients the relationship between PAI activity, insulin and other parameters. Patients showed higher level of PAI activity, as well as plasma glucose, insulin, triglyceride, cholesterol and Apolipoprotein B levels than normal controls; highest values were observed with diabetic patients also affected by coronary artery disease. A significant correlation was found between PAI activity and insulin (r = 0.60, p <0.001), body mass index (r = 0.32, p <0.05) and Apolipoprotein B (r = 0.33, p <0.05). The two latter correlations disappeared after adjustment for insulin.These results are in agreement with our previous report showing an in vitro effect of insulin on the synthesis of PAI by a hepatocellular cell line. Hyperinsulinemia presented by type 2 diabetic patients may increase the hepatic synthesis of PAI, inducing an hypofibrinolysis, which could play a role in the development of the vascular complications.Attempts to reduce hyperinsulinemia could have a favorable effect by lowering PAI activity.

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