Expression of plasminogen activator inhibitor-1 mRNA in healthy atherosclerotic and thrombotic human arteries and veins

Arnman, Veronika; Nilsson, Anders; Stemme, Sten; Risberg, Bo; Rymo, Lars

doi:10.1016/0049-3848(95)90180-n

Cited by 37 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PAI-1 has been immunohistochemically detected in endothelial cells, smooth muscle cells (SMC), and collagen fibers of atherosclerotic coronary artery [6]. Increased levels of PAI-1 mRNA were found in thrombotic human arteries compared to that in healthy arteries [7], Those findings imply that PAI-1 may play an important role in the devel opment of thrombosis and atherosclerosis.…”

Section: Introductionmentioning

confidence: 66%

G Proteins and Phospholipase C Mediate Thrombin-lnduced Generation of Plasminogen Activator Inhibitor-1 from Vascular Smooth Muscle Cells

Ren

Cockell²,

Fenton³

et al. 1997

J Vasc Res

View full text Add to dashboard Cite

The present study investigated transcellular signalling mechanism involved in thrombin-induced production of plasminogen activator inhibitor-1 (PAI-1) in cultured vascular baboon aortic smooth muscle cells (BASMC). Treatments with thrombin dose-dependently increased the steady state levels of PAI-1 mRNA and the generation of PAI-1 antigen from BASMC. Thrombin receptor-activating peptide mimicked the effect of thrombin on the generation of PAI-1. Sodium fluoride (1 mM) stimulated PAI-1 generation from BASMC. Pertussis toxin dose-dependently suppressed thrombin-induced increase of PAI-1 generation. Treatment with 5 mM neomycin, 10 µM U73122 or 1 µM calphostin C blocked thrombin-induced PAI-1 generation. Phorbol myristate acetate at 10 nM for 3 h strongly stimulated the generation of PAI-1 from BASMC. Forskolin (100 µM)or 8-bromo-cAMP (100 µM)suppressed thrombin-induced PAI-1 generation. The responses of quiescent BASMC to thrombin or the inhibitors on PAI-1 generation were comparable to that of growing cells. The results of the present study suggest that pertussis toxin-sensitive G proteins and a phospholipase C are involved in thrombin-induced generation of PAI-1 in BASMC, which may transmit signals from occupied thrombin receptor to protein kinase C and thereby increase the generation of PAI-1. Elevated levels of intracellular cAMP may negatively regulate the generation of PAI-1 from vascular SMC.

show abstract

Section: Introductionmentioning

confidence: 66%

G Proteins and Phospholipase C Mediate Thrombin-lnduced Generation of Plasminogen Activator Inhibitor-1 from Vascular Smooth Muscle Cells

Ren

Cockell²,

Fenton³

et al. 1997

J Vasc Res

View full text Add to dashboard Cite

show abstract

“…PAI-1 has been implicated in inflammation, endothelial dysfunction, and extracellular matrix remodeling (6). Increased levels of PAI-1 protein and mRNA were detected in atherosclerotic or thrombotic lesions in vasculature (3,52).…”

mentioning

confidence: 99%

Transmembrane signaling pathway mediates oxidized low-density lipoprotein-induced expression of plasminogen activator inhibitor-1 in vascular endothelial cells

Sangle

Zhao²,

Shen³

2008

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…Arterial endothelium normally controls a number of important functions vital to vascular health including vasodilation (11) and thromboresistance (4,10,27), which are related, respectively (in part), to nitric oxide (NO) and t-PA release. We hypothesized that the systemic process seen in acute coronary syndromes would extend to the peripheral circulation with reduced endothelium-dependent dilatation and t-PA release.…”

mentioning

confidence: 99%

Endothelial dysfunction occurs in peripheral circulation patients with acute and stable coronary artery disease

Thanyasiri

Celermajer

Adams

2005

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Thanyasiri, Panuratn, David S. Celermajer, and Mark R. Adams. Endothelial dysfunction occurs in peripheral circulation in patients with acute and stable coronary artery disease. Am J Physiol Heart Circ Physiol 289: H513-H517, 2005; doi:10.1152/ajpheart.01086.2004.-Atherosclerosis is a diffuse, systemic process. In addition, acute coronary syndromes (ACS) are associated with inflammatory marker elevations that are hypothesized to affect the function of nonculprit coronary as well as peripheral vessels. We investigated whether femoral vascular reactivity and/or fibrinolytic capacity are impaired in ACS patients over and above any dysfunction associated with stable coronary artery disease. Patients undergoing diagnostic coronary angiography (n ϭ 42 total, 14 patients/group) were recruited into three groups as follows: 1) stable coronary syndromes (SAP group), 2) ACS as defined by rest angina with ECG changes and troponin rise (ACS group), and 3) angiographically normal coronary arteries (control group). After diagnostic coronary angiography, femoral artery endothelial and smooth muscle function were assessed by infusing acetylcholine (ACh) and nitroglycerin (GTN), and tissue-type plasminogen activator (t-PA) release across the femoral circulation was measured as the difference between arterial and venous concentrations before and after ACh and GTN stimulation. There were no significant differences between groups in relevant baseline characteristics apart from significantly higher C-reactive protein levels and reduced net t-PA release in the ACS group at baseline (P Ͻ 0.05). The ACS and SAP groups had equivalent angiographic severity of coronary artery disease. Endothelium-dependent dilatation was significantly higher in control individuals (14.9 Ϯ 9.1%; P Ͻ 0.001) compared with either stable patients (2.3 Ϯ 8.1%) or those with unstable syndromes (2.6 Ϯ 8.9%, who were similar to each other; P ϭ not significant). Although baseline t-PA release was impaired in the ACS patients (0.09 Ϯ 0.06 compared with 0.39 Ϯ 0.33 and 0.49 Ϯ 0.56 ng/ml; P ϭ 0.03), stimulation of t-PA release by ACh and GTN occurred only in the control subjects and not in the ACS or SAP patients. Coronary artery disease is associated with impaired endothelium-dependent dilatation and impaired stimulation of t-PA release in the systemic circulation. These aspects of endothelial dysfunction, however, were equally severe in acute and chronic coronary syndrome patients.tissue-type plasminogen activator; nitroglycerin; acetylcholine; cardiac inflammation; thromboresistance; vasodilation ACUTE CORONARY SYNDROMES OCCUR when coronary atherosclerotic plaques become unstable with lesion rupture and/or subsequent thrombosis (12). In recent years, it has become apparent that this process is largely an inflammatory one that involves the interaction of leukocytes, cytokines, and endothelium (13). It has been hypothesized that this inflammatory activation with systemic cytokine release may lead to distant endothelial dysfunction in nonculprit coronary as well as per...

show abstract

Expression of plasminogen activator inhibitor-1 mRNA in healthy atherosclerotic and thrombotic human arteries and veins

Cited by 37 publications

References 25 publications

G Proteins and Phospholipase C Mediate Thrombin-lnduced Generation of Plasminogen Activator Inhibitor-1 from Vascular Smooth Muscle Cells

G Proteins and Phospholipase C Mediate Thrombin-lnduced Generation of Plasminogen Activator Inhibitor-1 from Vascular Smooth Muscle Cells

Transmembrane signaling pathway mediates oxidized low-density lipoprotein-induced expression of plasminogen activator inhibitor-1 in vascular endothelial cells

Endothelial dysfunction occurs in peripheral circulation patients with acute and stable coronary artery disease

Contact Info

Product

Resources

About