Investigating the relationship between the VNTR variant of the interleukin-1 receptor antagonist gene and coronary in-stent restenosis

Objective This study aimed to examine the association between the interleukin-1 receptor antagonist gene (IL-1RN) and coronary in-stent restenosis (ISR) through the analysis of the VNTR variant based on the previously reported results. Materials and methods The samples were classified into two clear...

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Published in:Molecular biology reports Vol. 50; no. 10; pp. 8575 - 8587
Main Authors: Klashami, Zeynab Nickhah, Mostafavi, Atoosa, Roudbordeh, Majid Gholamzadeh, Abbasi, Ali, Ebrahimi, Pirooz, Asadi, Mojgan, Amoli, Mahsa M.
Format: Journal Article
Language:English
Published: Dordrecht Springer Netherlands 01-10-2023
Springer Nature B.V
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Summary:Objective This study aimed to examine the association between the interleukin-1 receptor antagonist gene (IL-1RN) and coronary in-stent restenosis (ISR) through the analysis of the VNTR variant based on the previously reported results. Materials and methods The samples were classified into two clearly defined groups: the case group, which comprised 45 patients diagnosed with in-stent restenosis (ISR+), and the control group, which included 60 patients without ISR (ISR-). Polymerase chain reaction (PCR) was performed to examine the 86-bp VNTR variant of the IL-1RN gene. Results In the analysis of six identified groups consisting of variant alleles of 86 base pairs of VNTR of the IL-1RN gene statistically significant difference was observed for the presence of IL1RN*2 allele between cases and controls (p = 0.04, OR; 0.045). Conclusion Individuals with allele 2 of the IL-1Ra gene may be more predisposed to ISR. This could be due to an imbalance between IL-1Ra and IL-1β which is crucial in preventing the initiation or advancement of inflammatory diseases in specific organs. The observed phenomenon can be characterized by increased production of IL-1β and potential reduction of IL-1Ra as a result of functional VNTR variation in IL-RN gene.
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ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-023-08759-w