Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis

Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 Hin dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations....

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Veröffentlicht in:Clinical and experimental medicine 2009-09, Vol.9 (3), p.223-228
Hauptverfasser: Torres-Carrillo, Norma, Torres-Carrillo, Nora Magdalena, Martínez-Bonilla, Gloria Esther, Vázquez-Del Mercado, Mónica, Palafox-Sánchez, Claudia Azucena, Oregón-Romero, Edith, Bernard-Medina, Ana Guilaisne, Rangel-Villalobos, Héctor, Muñoz-Valle, José Francisco
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container_start_page 223
container_title Clinical and experimental medicine
container_volume 9
creator Torres-Carrillo, Norma
Torres-Carrillo, Nora Magdalena
Martínez-Bonilla, Gloria Esther
Vázquez-Del Mercado, Mónica
Palafox-Sánchez, Claudia Azucena
Oregón-Romero, Edith
Bernard-Medina, Ana Guilaisne
Rangel-Villalobos, Héctor
Muñoz-Valle, José Francisco
description Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 Hin dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 Hin dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed ( P  > 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference ( P  = 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers ( P  = 0.036). The PAI-1 Hin dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.
doi_str_mv 10.1007/s10238-009-0038-0
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Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 Hin dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 Hin dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed ( P  &gt; 0.05). 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Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 Hin dIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 Hin dIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed ( P  &gt; 0.05). RA patients showed lower PAI-1 plasma levels (18.92 ± 12.94 ng/ml) than CS (23.68 ± 23.38 ng/ml), without significant difference ( P  = 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 ± 13.81 ng/ml) with respect to C/C (16.77 ± 11.97 ng/ml) and G/G (10.47 ± 7.07 ng/ml) genotype carriers ( P  = 0.036). The PAI-1 Hin dIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>19238514</pmid><doi>10.1007/s10238-009-0038-0</doi><tpages>6</tpages></addata></record>
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subjects Arthritis, Rheumatoid - pathology
Deoxyribonuclease HindIII - metabolism
Disease Susceptibility
Enzyme-Linked Immunosorbent Assay - methods
Gene Frequency
Hematology
Humans
Internal Medicine
Medicine
Medicine & Public Health
Oncology
Original Article
Plasma - chemistry
Plasminogen Activator Inhibitor 1 - blood
Plasminogen Activator Inhibitor 1 - genetics
Polymerase Chain Reaction - methods
Polymorphism
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Protease inhibitors
Rheumatoid arthritis
title Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis
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