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A study of the possible association of plasminogen activator inhibitor type 1 4G/5G insertion/deletion polymorphism with susceptibility to schizophrenia and in its subtypes
Author(s) -
Yenilmez C.,
Ozdemir Koroglu Z.,
Kurt H.,
Yanas M.,
Colak E.,
Degirmenci I.,
Gunes H. V.
Publication year - 2017
Publication title -
journal of clinical pharmacy and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.622
H-Index - 73
eISSN - 1365-2710
pISSN - 0269-4727
DOI - 10.1111/jcpt.12470
Subject(s) - genotype , genotyping , allele , plasminogen activator inhibitor 1 , plasminogen activator , medicine , allele frequency , polymorphism (computer science) , genetics , microbiology and biotechnology , biology , gene
Summary What is known and objective Inhibition of the fibrinolytic system may occur at the level of plasminogen activation, mainly by PAI ‐1. Mental and physical stress caused to alterations of platelet function, and also decreased to fibrinolytic activity. Furthermore, stress‐induced thrombosis regulation was proposed to be by PAI ‐1 in schizophrenia patients. In this study, the distribution of genotypes and frequency of alleles of the plasminogen activator inhibitor type 1 ( PAI ‐1) gene 4G/5G polymorphism in different Turkish clinical schizophrenia subtypes was investigated for its role in schizophrenia development. Methods The clinical schizophrenia subtypes include paranoid, catatonic, disorganized, undifferentiated and residual, as diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders‐Fourth Edition IV ( DSM ‐ IV ). Samples of genomic DNA (250 total, including 150 schizophrenia patients and 100 healthy subjects) were analysed. PAI ‐1 4G/5G genotyping was performed by polymerase chain reaction–allele‐specific amplification. PCR products were separated by 2% agarose gel electrophoresis and then visualized. Results and discussion The genotype distributions ( P = 0·136) and allele frequencies ( P = 0·721 for 4G, P = 0. 097 for 5G) were not significantly different between patients with schizophrenia and control subjects for the 4G/5G polymorphism. Similar results were also found for the genotype distributions ( P = 0·640) and allele frequencies ( P = 0·763 for 4G, P = 0·448 for 5G) in the clinical schizophrenia subtypes compared to the each other. What is new and conclusion We conclude that PAI ‐1 4G/5G polymorphism was not significantly associated with schizophrenia or its subtypes in the Turkish population. However, we recognize that with our sample sizes, we cannot exclude weak associations.