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5-Hydroxytryptamine 5-HT2A receptor and 5-hydroxytryptamine transporter polymorphisms in acute myocardial infarction.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Coto, Eliecer Reguero, J. Rodríguez Álvarez, V. González Morales, Blanca Batalla, Alberto González, Pelayo Martín, María Carolina García-Castro, Mónica Iglesias-Cubero, Gustavo Cortina, Arturo |
| Copyright Year | 2003 |
| Abstract | This study was designed to analyse possible associations between DNA polymorphisms in the 5-hydroxytryptamine (5-HT; serotonin) 5-HT(2A) receptor and the 5-HT transporter (5-HTT) genes, and myocardial infarction (MI). 5-HT has been shown to be involved in cardiovascular pathophysiology. In addition to platelet aggregation and vascular contraction, 5-HT induces hyperplasia of artery smooth muscle cells. Recently, a 5-HT transporter gene polymorphism has been associated with MI. To determine the influence of genetic variation at the 5-HT(2A) receptor (T102C polymorphism) and the 5-HTT (insertion/deletion polymorphism) on the risk of developing early MI, we genotyped 210 MI patients of < 55 years old and 238 healthy control subjects for DNA polymorphisms in these genes. In addition, we genotyped 95 patients with late-onset MI (> 60 years old) to analyse the effects of these polymorphisms on the age at which the first MI episode occurred. The 5-HT(2A) receptor polymorphism was not associated with MI in our population. In addition, since the 5-HT(2A) receptor gene and genotype frequencies did not differ between patients with early and late onset of MI, this polymorphism does not appear to have an effect on age at the first MI episode. Gene and genotype frequencies for the 5-HTT promoter did not differ between patients < 55 years old and healthy controls (independent of smoking status). However, homozygotes for the deletion (the ss genotype, where s denotes the short allele) were present at a significantly higher frequency in patients >60 years old compared with patients < 55 years old (P = 0.009; P = 0.004 when only smokers were compared). According to our data, the ss genotype would seem to have a protective role against MI, delaying the age of onset of the first episode, especially among smokers. This could be a consequence of the lower 5-HTT levels linked to the s allele, so that individuals homozygous for the ss genotype may have lower 5-HT re-uptake by platelets. |
| Starting Page | 20 |
| Ending Page | 28 |
| Page Count | 9 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.clinsci.org/content/ppclinsci/104/3/241.full.pdf |
| PubMed reference number | 12605580v1 |
| Volume Number | 104 |
| Issue Number | 3 |
| Journal | Clinical science |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Artery Smooth Muscle Tissue Blood Platelet Disorders Blood Platelets Deletion Mutation Genetic Polymorphism Hereditary Diseases Homozygote Insertion Mutation Mental association Muscle Cells Myocardial Infarction Myocytes, Smooth Muscle Patients Receptor, Serotonin, 5-HT2A Serotonin Smooth muscle (tissue) Status Epilepticus |
| Content Type | Text |
| Resource Type | Article |