Association of plasminogen activator inhibitor-1 gene polymorphism with inflammatory bowel disease in Iranian Azeri Turkish patients

Abstract

Background/Aim:Previous studies have shown the association of some genetic factors, such as Plasminogen activator inhibitor type-1 (PAI-1) 4G/5G polymorphism, with the development of inflammatory bowel disease (IBD). We aimed to study this polymorphism as a risk factor in IBD patients in this cohort.Patients and Methods:One hundred and fifteen IBD patients and 95 healthy controls were selected from Iranian Azeri Turks and -6754G/5G polymorphism of PAI-1 gene was tested by polymerase chain reaction using allele-specific primers confirmed by sequencing.Results:There was no significant difference of PAI-1 polymorphism between IBD patients and the control group (P > 0.05). Furthermore, these data showed no significant difference between Crohn's disease and ulcerative colitis patients. However, 4G/4G homozygotes have reduced probability to progression of loss of appetite, whereas 5G/5G genotypes have increased risk for development of chronic diarrhea without blood, nausea, and loss of appetite.Conclusions:Although our study showed no significant association of PAI-1 polymorphism between patients and control group, the carriers of 4G/4G genotype and 4G allele had reduced risk for the progression of IBD features in this cohort.

Identification of Candidate Genes Related to Inflammatory Bowel Disease Using Minimum Redundancy Maximum Relevance, Incremental Feature Selection, and the Shortest-Path Approach

“…Tissue plasminogen activator and urokinase are both associated with inflammation and the process of wound healing [ 124 ]. SERPINE1 and proteins in the downstream of its specific pathway have also been reported to be directly associated with IBD as a functional regulator [ 125 , 126 ]. As a candidate gene, we also predicted an angiogenesis-associated gene VEGFC , which regulates angiogenesis and endothelial cell growth [ 127 , 128 ].…”

V617F‐independent upregulation of JAK2 gene expression in patients with inflammatory bowel disease

“…30 Therefore, seems that the lack of JAK2 V617F mutation in our study was due to the small samples of patients with IBD having thromboembolism, who none of them had MPN complication, or this mutation in patients with IBD is low. Also, several studies have shown the role of other factors in the pathogenesis of IBD's thrombosis such as fibrinolysis system, 10,31-33 plasma coagulation inhibitors, 31,34,35 homocysteine, 31,36,37 platelet disorders, 31,38,39 autoantibodies, 9,40 and genetic factors [such as Factor Ⅴ Leiden G1691A mutation, 41 pro-thrombin G20210A muta-tion, 42 methylene-tetra-hydrofolate reductase C677T mutation, 43 and plasminogen activator inhibitor type 1 (PAI-1) mutation 44 .…”