The Regulatory Variant -108C/T in the Promoter of Paraoxonase 1 (PON1) Gene has a More Important Role in Regulating PON1 Activity Compared to rs3735590 in 3'-UTR in Patients with Coronary Artery Disease.

Coronary artery disease PON1 single-nucleotide variation

Journal

Advanced biomedical research
ISSN: 2277-9175
Titre abrégé: Adv Biomed Res
Pays: India
ID NLM: 101586897

Informations de publication

Date de publication:
2024
Historique:
received: 17 11 2022
revised: 20 02 2024
accepted: 02 03 2024
medline: 3 9 2024
pubmed: 3 9 2024
entrez: 3 9 2024
Statut: epublish

Résumé

This study aimed to assess the serum activity of paraoxonase 1 (PON1) in patients with coronary artery disease (CAD) based on two genetic variants including the -108C/T variant in the promoter region and the rs3735590 variant in the binding site of miR-616 at the 3'-UTR of the PON1 gene. A total of 140 subjects who exhibited clinical symptoms of CAD underwent diagnostic coronary angiography. The patients with CAD were further categorized into two groups: single-vessel disease (SVD) and multi-vessel disease (MVD). The study variants were genotyped using the restriction fragment length polymorphism (RFLP) technique after polymerase chain reaction amplification. After adjusting for age, gender, body mass index, metformin, and statin usage, a significant association was observed between the -108C/T variant and PON1 activity ( Our study findings indicate a significant decrease in PON1 activity among patients with obstructive CAD. Notably, our results suggest that the -108C/T variant exerts a greater influence on PON1 activity compared to the rs3735590 variant. These findings highlight the crucial role of the -108C/T variant in modulating PON1 activity within the context of atherosclerosis.

Sections du résumé

Background UNASSIGNED
This study aimed to assess the serum activity of paraoxonase 1 (PON1) in patients with coronary artery disease (CAD) based on two genetic variants including the -108C/T variant in the promoter region and the rs3735590 variant in the binding site of miR-616 at the 3'-UTR of the PON1 gene.
Materials and Methods UNASSIGNED
A total of 140 subjects who exhibited clinical symptoms of CAD underwent diagnostic coronary angiography. The patients with CAD were further categorized into two groups: single-vessel disease (SVD) and multi-vessel disease (MVD). The study variants were genotyped using the restriction fragment length polymorphism (RFLP) technique after polymerase chain reaction amplification.
Results UNASSIGNED
After adjusting for age, gender, body mass index, metformin, and statin usage, a significant association was observed between the -108C/T variant and PON1 activity (
Conclusions UNASSIGNED
Our study findings indicate a significant decrease in PON1 activity among patients with obstructive CAD. Notably, our results suggest that the -108C/T variant exerts a greater influence on PON1 activity compared to the rs3735590 variant. These findings highlight the crucial role of the -108C/T variant in modulating PON1 activity within the context of atherosclerosis.

Identifiants

pubmed: 39224397
doi: 10.4103/abr.abr_391_22
pii: ABR-13-38
pmc: PMC11368222
doi:

Types de publication

Journal Article

Langues

eng

Pagination

38

Informations de copyright

Copyright: © 2024 Advanced Biomedical Research.

Déclaration de conflit d'intérêts

There are no conflicts of interest.

Auteurs

Mehryar Zargari (M)

Molecular and Cell Biology Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
Department of Clinical Biochemistry and Medical Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Negar Maadi (N)

Department of Clinical Biochemistry and Medical Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Maysam Rezapour (M)

Department of Paramedicine, Amol Paramedical Sciences School, Mazandaran University of Medical Sciences, Sari, Iran.

Abouzar Bagheri (A)

Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran.

Samane Fallahpour (S)

Department of Clinical Biochemistry and Medical Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Mani Nosrati (M)

Department of Clinical Biochemistry and Medical Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.

Abdolkarim Mahrooz (A)

Molecular and Cell Biology Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
Department of Clinical Biochemistry and Medical Genetics, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran.

Classifications MeSH