PAI-1 Plasma Levels in a General Population Without Clinical Evidence of Atherosclerosis

Margaglione, Maurizio; Cappucci, Giuseppe; d’Addedda, Marina; Colaizzo, Donatella; Giuliani, Nicola; Vecchione, Gennaro; Mascolo, Giulio; Grandone, Elvira; Minno, Giovanni Di

doi:10.1161/01.atv.18.4.562

Cited by 141 publications

(111 citation statements)

References 49 publications

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“…It has been suggested that this single base-pair polymorphism 675-bp upstream from the start of transcription is functionally important in regulating the expression of the PAI-1 gene and the 4G allele has been associated with increased PAI-1 activity. 10,17 Also chronic smoking has been associated with impaired fibrinolysis in plasma and this largely reflected elevated plasma PAI-1 in smokers. 14 It is interesting that the genetic association of the functional promoter polymorphism in the PAI-1 gene with periodontitis in our study was observed only in the group of non-smokers.…”

Section: Genes and Immunitymentioning

confidence: 99%

Plasminogen-activator-inhibitor-1 promoter polymorphism as a risk factor for adult periodontitis in non-smokers

et al. 2002

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Periodontal diseases belong to the most common chronic disorders affecting mankind. Smoking and impaired plasminogen activation with hypercoagulation and fibrinolysis inhibition have been proposed as having a role in predisposition to these diseases. We investigated relationships among adult periodontitis, smoking, and a variation in the deletion/insertion (4G/5G) promoter polymorphism of the plasminogen-activator-inhibitor-1 (PAI-1) gene in 304 Caucasian subjects. An association was detected between the deletion (4G) allele (and 4G/4G genotype)

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Section: Genes and Immunitymentioning

confidence: 99%

Plasminogen-activator-inhibitor-1 promoter polymorphism as a risk factor for adult periodontitis in non-smokers

et al. 2002

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“…Since the levels of the selected markers are increased in smokers (Eliasson et al, 1995;de Maat et al, 1996, Miller et al, 1998Margaglione et al, 1998), we hypothesized that reduction of the oxidative stress by tea polyphenols may normalize the increased levels.…”

Section: Introductionmentioning

confidence: 96%

Consumption of black and green tea has no effect on inflammation, haemostasis and endothelial markers in smoking healthy individuals

Maat¹,

Pijl

Kluft³

et al. 2000

Eur J Clin Nutr

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Obejective: Firstly, to study the effect of tea and tea polyphenols on cardiovascular risk indicators of the in¯ammatory system (IL6, IL1b and TNF-a, CRP), and on haemostasis and endothelial proteins with an acute phase behaviour (®brinogen, vWF, PAI-1, FVIIa and u-PA). Secondly, to study the relationship between plasma levels of antioxidants (a-tocopherol, b-carotene and vitamin C) and these acute-phase, cardiovascular risk indicators. Design: Randomized study. Subjects: Sixty-four smoking healthy volunteers were recruited by newspaper advertisements; there were ®ve dropouts. Intervention: Four-week administration of black tea, green tea, green tea polyphenol isolate and mineral water (13 ± 16 per group). Measures: Plasma levels of the in¯ammatory markers IL6, IL1b, TNF-a, CRP, ®brinogen, vWF, PAI-1, FVIIa and u-PA and of the antioxidants a-tocopherol, b-carotene and vitamin C. Results: Different dosages of tea polyphenols had no effect on in¯ammation, haemostasis and endothelial markers. There was a signi®cant negative correlation between the levels of the antioxidant b-carotene and the in¯ammation markers IL6 and ®brinogen (r 70.35 and r 70.37, respectively, P`0.01) in this group of smokers. Remarkably, there was a signi®cant positive correlation between the levels of the antioxidant atocopherol and the in¯ammation marker IL6 (r 0.28, P`0.05). Conclusions: Tea drinking had no effect on the levels of the in¯ammation, haemostasis and endothelial cardiovascular risk factors measured. We did observe a relationship between the antioxidant variables atocopherol and b-carotene and in¯ammation markers in this group of healthy smoking subjects. Sponsorship: This work was supported in part by

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“…Under conditions of cytokine stimulation, the 4G allele had higher activity than the 5G allele. 1 Accordingly, the 4G allele was related to higher plasma PAI-1 antigen levels or activity in most [2][3][4][5] but not all 6 studies in non-Hispanic white populations. However, studies including different ethnic groups, such as Afro-Caribbeans, 7 Asians, 7 Pima Indians, 8 or Japanese, 9 have reported different frequencies of the 4G allele from those in non-Hispanic whites, as well as differences in the relation of the 4G/5G genotype to circulating levels of PAI-1.…”

mentioning

confidence: 94%

Promoter (4G/5G) Plasminogen Activator Inhibitor-1 Genotype and Plasminogen Activator Inhibitor-1 Levels in Blacks, Hispanics, and Non-Hispanic Whites

et al. 2003

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Background-The 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene has been related to cardiovascular disease. Methods and Results-Insulin resistance was measured with a frequently sampled intravenous glucose tolerance test in the Insulin Resistance Atherosclerosis Study (IRAS), and PAI-1 4G/5G promoter genotype was established by allelespecific polymerase chain reaction amplification of genomic DNA. There were 287 subjects with the 4G/4G genotype (18.4%), 691 heterozygote subjects (44.2%), and 586 carriers of the 5G/5G genotype (37.5%). The genotype distribution was different across the 3 ethnic groups (Pϭ0.001). PAI-1 levels were lower in blacks than in non-Hispanic whites and Hispanics and lower in non-Hispanic whites than in Hispanics (all Pϭ0.0001). Subjects homozygous for the 4G allele had the highest plasma PAI-1, heterozygote subjects were intermediate, and 5G homozygotes had the lowest levels of PAI-1. These patterns remained unaffected by adjustments for age, gender, clinical center, glucose tolerance status, body mass index, waist, triglycerides, and insulin resistance. Multiple linear regression analyses showed that the 4G/5G genotype explained very little of the variation in PAI-1 levels (0.63% in non-Hispanic whites, 0.99% in Hispanics, and 2.37% in blacks), and interaction analyses revealed no significant differences in the relation of circulating PAI-1 levels to the 4G/5G genotype by ethnicity (Pϭ0.4). Conclusions-We have shown ethnic differences in the PAI-1 4G/5G polymorphism along with corresponding differences in circulating PAI-1 levels. The association of the genotype with PAI-1 levels was seen consistently among all 3 ethnic groups and was unaffected by metabolic covariates, including insulin resistance. (Circulation. 2003;107:2422-2427.)

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PAI-1 Plasma Levels in a General Population Without Clinical Evidence of Atherosclerosis

Abstract: Abstract-Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels.

Cited by 141 publications

References 49 publications

Plasminogen-activator-inhibitor-1 promoter polymorphism as a risk factor for adult periodontitis in non-smokers

Plasminogen-activator-inhibitor-1 promoter polymorphism as a risk factor for adult periodontitis in non-smokers

Consumption of black and green tea has no effect on inflammation, haemostasis and endothelial markers in smoking healthy individuals

Promoter (4G/5G) Plasminogen Activator Inhibitor-1 Genotype and Plasminogen Activator Inhibitor-1 Levels in Blacks, Hispanics, and Non-Hispanic Whites

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