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

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Abstract

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 HindIII 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 HindIII 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 HindIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.

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Acknowledgments

This work was supported by grant no. 45703-M to JFMV of the National Council of Science and Technology (CONACyT, México-Universidad de Guadalajara).

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The authors declare that they have no conflict of interest related to the publication of this manuscript.

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Correspondence to José Francisco Muñoz-Valle.

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Torres-Carrillo, N., Torres-Carrillo, N.M., Martínez-Bonilla, G.E. et al. Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis. Clin Exp Med 9, 223–228 (2009). https://doi.org/10.1007/s10238-009-0038-0

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  • DOI: https://doi.org/10.1007/s10238-009-0038-0

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