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Myocardial infarction is associated with Spl binding site polymorphism of collagen type 1A1 gene
Gábor Speer1, Péter Szenthe, János P Kósa
11st Department of Medicine, Semmelweis University, Budapest, Hungary. speerga@bel1.sote.hu
Insights
The collagen type 1A1 (COL1A1) gene Sp1 polymorphism, specifically the "SS" genotype, was more frequent in myocardial infarction (MI) survivors. Cardiovascular risk factors were higher in carriers of the "s" allele, suggesting a potential role in MI development.
Area of Science:
- Cardiovascular Genetics
- Molecular Biology
- Atherosclerosis Research
Background:
- Collagen type I is present in atherosclerotic lesions, influencing plaque stability, but absent in normal coronary arteries.
- The collagen type 1A1 (COL1A1) gene Sp1 binding site (-1245 G/T) polymorphism is linked to altered collagen production.
- Understanding genetic predispositions is crucial for cardiovascular disease research.
Purpose of the Study:
- To investigate the association between COL1A1 gene Sp1 polymorphism and myocardial infarction (MI).
- To explore the relationship between this polymorphism and cardiovascular risk factors in MI patients.
Main Methods:
- Genotyping for COL1A1 gene Sp1 polymorphism (-1245 G/T) in 136 MI patients and 212 controls.
- Assessment of cardiovascular risk factors including serum adiponectin, insulin status, and lipid profiles.
Main Results:
- The 'SS' genotype of COL1A1 was significantly more prevalent in MI survivors compared to controls.
- 'Ss' and 'ss' genotypes (presence of the 's' allele) were less frequent in MI patients.
- Carriers of the 's' allele exhibited a higher incidence of cardiovascular risk factors than 'S' allele carriers.
Conclusions:
- The COL1A1 gene Sp1 polymorphism may influence the development of myocardial infarction.
- This genetic variation could be a contributing factor to cardiovascular disease risk.
Objective:
Human atherosclerotic lesions contain collagen type I, which plays a pivotal role in atherosclerotic plaque stability. In contrast, the normal coronary arteries do not express this type of collagen. Data have shown that the collagen type 1A1 (COL1A1) gene Sp1 binding site (-1245 G/T) polymorphism is associated with disturbed collagen protein production.
Methods:
In our study, COL1A1 gene Sp1 polymorphism was investigated in 136 patients with myocardial infarction (MI) 5 months after the acute phase, and 212 age-matched control subjects in association with any cardiovascular risk factors (such as serum adiponectin levels, hyperinsulinaemic status, hyperlipaemia).
Results:
The "SS" genotype of the COL1A1 gene was found to occur significantly more frequently in patients surviving a MI, as compared to the control group and the "Ss" and "ss" genotype frequencies (the presence of the s allele) were lower in our patients, than in control group. However, the occurrence of cardiovascular risk factors was significantly higher among the "s" allelic carriers as compared to patients carrying the "S" allele of the COL1A1 gene.
Conclusion:
Our results raise the possibility that COL1A1 gene Sp1 polymorphism might have an impact on the development of MI.
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