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Lack of association between Ser(413)/Cys polymorphism of plasminogen activator inhibitor type 2 (PAI-2) and premature coronary atherosclerotic disease

Plasminogen activator inhibitor type-2 (PAI-2) is a serine protease inhibitor of the fibrinolytic system produced predominantly by the macrophages and monocytes. It has been demonstrated that fibrinolysis regulation has a great importance in the pathogenesis of atherosclerotic plaques. Thus in the c...

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Detalles Bibliográficos
Autores principales: Saffari, Babak, Jooyan, Najmeh, Bahari, Marzieh, Senemar, Sara, Yavarian, Majid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Leibniz Research Centre for Working Environment and Human Factors 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942808/
https://www.ncbi.nlm.nih.gov/pubmed/27418916
Descripción
Sumario:Plasminogen activator inhibitor type-2 (PAI-2) is a serine protease inhibitor of the fibrinolytic system produced predominantly by the macrophages and monocytes. It has been demonstrated that fibrinolysis regulation has a great importance in the pathogenesis of atherosclerotic plaques. Thus in the current investigation, we sought to determine whether Ser(413)/Cys polymorphism (rs6104) of PAI-2 gene could be associated with atherosclerosis and cardiovascular risk factors. Ser(413)/Cys polymorphism was determined by PCR-RFLP technique using Mwo I restriction enzyme for 184 men under 50 years of age and 216 women less than 55 years of age who underwent diagnostic coronary angiography. Data on the history of familial myocardial infarction or other heart diseases, hypertension, and smoking habit were collected by a simple questionnaire. Fasting levels of blood sugar, triglycerides, total cholesterol, low-density lipoprotein and high-density lipoprotein cholesterol levels were also measured by enzymatic methods. Frequencies of the Ser(413) and Cys(413) alleles were 0.760 and 0.240 in the whole population, respectively. The PAI-2 gene variant analyzed was not significantly associated with either the prevalence of premature CAD or the classical risk factors of CAD development such as diabetes, serum cholesterol, triglycerides, low-density lipoprotein and high-density lipoprotein cholesterol, body mass index, hypertension, familial history of heart dysfunction or smoking.