Plasminogen Activator Inhibitor 1 and Atherothrombosis

Juhan‐Vague, I.; Alessi, Marie‐Christine

doi:10.1055/s-0038-1646175

Cited by 191 publications

(89 citation statements)

References 116 publications

(70 reference statements)

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“…The role of PAI-1 as a fibrinolytic inhibitor 36 appears clinically important, with elevations associated with venous thrombosis 36 and myocardial infarction. 37,38 In the present study, a 25% reduction in PAI-1 activity was observed after 6 weeks of combined HRT, consistent with other prospective studies using either estrogen alone or combined HRT 14,16 -18,39 and indicating that HRT with estradiol and norethisterone increases plasma fibrinolytic inhibitory activity.…”

Section: Discussionsupporting

confidence: 80%

Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis

Teede

McGrath

Smolich

et al. 2000

ATVB

124

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Abstract-Hormone replacement therapy (HRT) appears to be cardioprotective in postmenopausal women; however, concerns exist over its thrombogenic effects. To address the effects of combined HRT on coagulation and fibrinolysis, we have measured circulating markers of these processes in a double-blind placebo-controlled trial. Forty-two healthy postmenopausal women aged 50 to 75 years received continuous combined HRT with 2 mg estradiolϩ1 mg norethisterone or placebo for 6 weeks. Hormone profiles were measured at baseline, and lipid and hemostatic parameters were measured at baseline and after 6 weeks of therapy. Baseline characteristics were similar in the 2 groups. With change from baseline the main outcome measure, HRT increased the markers of coagulation (prothrombin fragments 1ϩ2, 0.

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Section: Discussionsupporting

confidence: 80%

Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis

Teede

McGrath

Smolich

et al. 2000

ATVB

124

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“…These results showed several novel aspects of CRP functions in the vascular system. PAI-1 is a key regulator of fibrinolysis through inhibiting tissue and/or urokinase plasminogen activator [16]. Our data clearly indicate that CRP upregulates PAI-1 expression in both mRNA and protein levels in HCAEC.…”

Section: Discussionsupporting

confidence: 51%

“…PAI-1 expression is highly regulated by many factors including cytokines, oxidative stress, and cellular signaling molecules such as mitogen-activated protein kinases (MAPKs). The elevated PAI-1 is closely associated with enhanced thrombosis by impairing fibrinolysis [14][15][16][17][18], which has been recognized as an important risk factor for atherosclerotic vascular disease [15]. However, it is not fully understood whether CRP could affect PAI-1 expression in different endothelial cells though a unique molecular mechanism.…”

Section: Introductionmentioning

confidence: 99%

C-reactive protein increases plasminogen activator inhibitor-1 expression in human endothelial cells

Chen

Nan

Lin

et al. 2008

Thrombosis Research

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C-reactive protein (CRP) is an inflammatory marker which predicts cardiovascular disease. However, it is not fully understood whether CRP has direct effects on endothelial functions and gene expression. The purpose of current study was to determine the effects and molecular mechanisms of CRP on the expression of plasminogen activator inhibitor-1 (PAI-1) in human endothelial cells. Human coronary artery endothelial cells (HCAEC) were treated with CRP at clinically relevant concentrations for different durations. PAI-1 mRNA, protein and enzyme activities were studied. The effects of CRP on MAPK p38 phosphorylation was also studied by Bio-Plex luminex immunoassay. In addition, other types of human endothelial cells isolated from umbilical vein, skin, and lung microvessels were tested. CRP significantly increased PAI-1 mRNA levels in a time-and concentration-dependent manner. The protein level and enzyme activity of PAI-1 in the supernatant of CRP-treated HCAEC cultures were significantly increased. Anti-CD32 antibody effectively blocked CRP-induced PAI-1 mRNA expression. In addition, CRP significantly increased CD32 mRNA levels and enhanced phosphorylation of MAPK p38. Furthermore, antioxidant curcumin dramatically inhibited CRP-induced PAI-1 mRNA expression. The effect of CRP on PAI-1 expression was also confirmed in other types of human endothelial cells. In conclusion, CRP significantly increased the expression of PAI-1 in HCAEC and other human endothelial cells. CRP also increased its receptor CD32 expression which may further enhance its action. CRP-induced PAI-1 expression may be mediated by oxidative stress and p38 signal pathway as antioxidant effectively blocks the effect of CRP on HCAEC.

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“…Recently Raikkijnen et a1 (27) showed that chronic stress, defined as feelings of fatigue, lack of energy, increased irritability, and demoralization, was positively associated with plasminogen activator inhibitor-1 (PAI-1) antigen (27), while deficient fibrinolysis, due to an increase in PAI-1, may be involved in thrombosis (28). Approximately 3 1 % of the subjects in our study were receiving the drug gemfibrozil, a fibrate derivative designed for CHD prevention by modulation of serum lipid levels.…”

mentioning

confidence: 99%

Shift work, occupation and coronary heart disease over

Tenkanen¹,

Sjöblom²,

Kalimo³

et al. 1997

Scand J Work Environ Health

166

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ObjectivesThe risk of coronary heart disease (CHD) in shift work and the possible pathways for CHD in industrial workers were studied along with the importance of shift work as an occupational class gradient of CHI) risk. Methods Data from a psychosocial questionnaire and on life-style factors, blood pressure, and serum lipid levels were used for a follow-up study of a cohort of 1806 workers. CHD was determined from official Fi~~nish registers. Cox's proportional hazards models were used with different covariates to evaluate the relative rislcs associated with shift work. Results All the blue-collar workers smoked more and a had higher systolic blood pressure than the whitecollar workers. Three-shift workers scored low for job-decision latitude on the Karasek job stress scales. There were no differences in the total cholesterol or high-density lipoprotein cholesterol levels. When all the shift workers were compared with all the day workers, the relative risk of CHD was 1.5 [95% confidence interval (95% CI) 1.1-2.11 when only age was adjusted for and 1.4 (95% CI 1.0-1.9) when life-style factors, blood pressure, and serum lipids were also adjusted for. The blue-collar day workers and 2-shift and 3-shift workers had relative risks of 1.3 (95% CI 0.8-2.0), 1.9 (95% CI 1.1-3.4), and 1.7 (95% CI 1.1-2.7), respectively, when compared with the white-collar day workers. C O~C~U S~O~S Shift work is an important part of the occupational gradient in CHD risk among industrial workers; some evidence was found for the hypothesis that a direct stress-related mechanism explains part of the increased CHD risk.Key terms blood pressure, coronary heart disease, job stress, life-style, occupation, shift work.While most occupational health hazards have been strongly curtailed in Western industrialized countries, shift work remains common. In fact, the number of shift workers has even increased in some branches of industry, for example, in manufacturing (1). The total number of night and shift workers seems to be between some 15% and 20% of the total working population in most European Community countries (1). Approximately 20% of shift workers are forced to move to day work during their first year of employment due to disturbances in their circadian rhythm, with accompanying sleep disturbances, difficulties in social life, and various stress reactions (2). Even those who accommodate may nevertheless be at increased risk of long-term health hazards. Whether or not shift workers are at increased risk of coronary heart disease (CHD) has been studied since the middle of the century with contrasting findings. In 1978 Harrington (3) concluded in his review that there was no conclusive evidence for an increased incidence of cardiovascular disorders for shift workers. After the followup study of Knutsson et a1 (4) and the massive aggregated data study by Alfredsson et a1 (3, Waterhouse and his colleagues (6) found, in their review from 1992, that the evidence in favor of an increased risk of CHD in association with shift work is becoming more...

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Plasminogen Activator Inhibitor 1 and Atherothrombosis

Cited by 191 publications

References 116 publications

Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis

Postmenopausal Hormone Replacement Therapy Increases Coagulation Activity and Fibrinolysis

C-reactive protein increases plasminogen activator inhibitor-1 expression in human endothelial cells

Shift work, occupation and coronary heart disease over

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