scholarly journals C-Reactive Protein Increases Plasminogen Activator Inhibitor-1 Expression and Activity in Human Aortic Endothelial Cells

Circulation ◽  
2003 ◽  
Vol 107 (3) ◽  
pp. 398-404 ◽  
Author(s):  
Sridevi Devaraj ◽  
Dan Yan Xu ◽  
Ishwarlal Jialal
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
C Reactive Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Aortic Endothelial Cells ◽  
Reactive Protein ◽  
Human Aortic Endothelial Cells ◽  
Activator Inhibitor ◽  
Expression And Activity

Atrial Natriuretic Peptide Inhibits the Expression of Tissue Factor and Plasminogen Activator Inhibitor 1 Induced by Angiotensin II in Cultured Rat Aortic Endothelial Cells

1998 ◽  
Vol 79 (03) ◽  
pp. 631-634 ◽  
Author(s):  
Hajime Tsuji ◽  
Hiromi Nishimura ◽  
Teruhisa Kasahara ◽  
Tatsuya Sugano ◽  
Haruchika Masuda ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Ang Ii ◽  
Plasminogen Activator Inhibitor 1 ◽  
Aortic Endothelial Cells ◽  
Activator Inhibitor ◽  
Pai 1

SummaryThe pharmacological characteristics of atrial natriuretic peptide (ANP), such as natriuresis, vasodilation, or suppression of smooth muscle cell proliferation, are well investigated. However, this is the first study to report its role on blood coagulation and fibrinolysis mediated by vascular endothelial cells. In this study, the effects of ANP on the enhanced expression of tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) by angiotensin II (Ang II) in cultured rat aortic endothelial cells (RAECs) were examined. The expressions of TF and PAI-1 mRNA were detected by northern blotting methods. The activities of TF on the surface of RAECs and PAI-1 in the culture media were measured by chromogenic assay. ANP suppressed mRNA expressions of TF and PAI-1 induced by Ang II in a concentration-dependent manner. This suppression was accompanied by the decreased activities of TF and PAI-1.

scholarly journals Defining the Proinflammatory Phenotype Using High Sensitive C-Reactive Protein Levels as the Biomarker

2005 ◽  
Vol 90 (8) ◽  
pp. 4549-4554 ◽  
Author(s):  
Sridevi Devaraj ◽  
Grant O’Keefe ◽  
Ishwarlal Jialal
Keyword(s):  
Cell Adhesion ◽  
Plasminogen Activator ◽  
Body Mass ◽  
Whole Blood ◽  
Plasminogen Activator Inhibitor ◽  
C Reactive Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Reactive Protein ◽  
Tnf Α ◽  
Activator Inhibitor

Context: Inflammation is pivotal in atherosclerosis. The prototypic marker of inflammation is C-reactive protein (CRP). Numerous studies have confirmed that high CRP levels in normal volunteers predict cardiovascular events. Objective: The objective of this study was to define proximal and associated abnormalities of the proinflammatory phenotype using CRP levels as the biomarker. Design and Subjects: Two groups of normal, healthy subjects, selected by stringent criteria from an initial cohort of 252, were studied over the period of 12 months. Group 1 included subjects with consistently low CRP (<0.004 μm or <0.5 mg/liter; low CRP group; n = 15). Group 2 included subjects with consistently high CRP (>2.0 or >0.016 μm to <10 mg/liter or <0.085 μm; high CRP group; n = 13). Main Outcome Measures: Fasting blood (50 ml) was obtained, and the following parameters were assayed: high sensitivity CRP, fibrinogen, lipid profile, insulin, whole blood cytokines after stimulation with lipopolysaccharide (LPS; 100 ng/ml for 24 h), soluble cell adhesion molecules, plasminogen activator inhibitor-1, CD40, CD40 ligand, leptin, adiponectin, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-3 (MMP-3), and MMP-9. Genomic DNA was obtained from peripheral blood leukocytes, and the TNF-α −308 genotype was determined. Results: The median CRP levels were 0.0018 μm (0.21 mg/liter) and 0.031 μm (3.7 mg/liter) for the low and high groups, respectively. High CRP subjects were older and had significantly higher body mass indexes, triglycerides, insulin, homeostasis model assessment, and leptin levels compared with low CRP subjects. The markers of inflammation, plasminogen activator inhibitor-1, MMP-9, fibrinogen, and vascular cell adhesion molecule-1 levels were significantly higher in the high compared with the low CRP group. LPS-stimulated levels of whole blood IL-1β, IL-6, and TNF were significantly higher, and IL-4 levels were significantly lower in the high CRP group. After age- and body mass index-adjusted analysis of covariance, only plasma MMP-9 levels and LPS-stimulated whole blood IL-1β and TNF levels were significantly higher in the high CRP group. The frequency of the rare A allele at TNF-α −308 was equivalent in high and low CRP groups. Conclusions: A phenotype characterized by increased plasma inflammatory mediators as well as increased LPS-stimulated whole blood TNF-α and IL-1β levels is associated with high plasma CRP levels. This systemic inflammatory phenotype may contribute to vascular inflammation or may reflect inflammation in vessels or at other sites.

Sign in / Sign up

Export Citation Format

Share Document