title: Lipid profile and inflammatory markers associated with estrogen receptor alpha PvuII and XbaI gene polymorphisms.
abstract: Estrogen is established to influence lipoprotein metabolism and inflammatory markers. Alternations in estrogen receptor alpha (ESR1) expression and function may affect the role of estrogen in this regard. The aim of this study was to determine whether ESR1 PvuII and XbaI gene polymorphisms have effects on lipoprotein (a) as well as inflammatory variables in an Iranian population. Three hundred and ninety seven consecutive participants (228 men, 57.4%) who were admitted at our center for elective coronary angiography because of symptoms related to coronary artery disease (CAD) were enrolled in our study. Total cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride levels were determined by standard methods using commercial kits. Low-density lipoprotein (LDL)-cholesterol was calculated according to the Friedewald formula. The lipoprotein (a) levels were measured by ELISA method using Biopool kit, and the CRP concentrations were determined by Latex Immunoturbidometry. The presence of PvuII and XbaI polymorphisms within the ESR gene were analyzed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP). The frequency of homozygous and heterozygous were 25.9% and 50.1%, for PvuII genotypes, and the frequency was 23.7% and 48.6%, for XbaI genotypes, respectively. After adjusting for CAD and age, no impacts of ESR1 PvuII and XbaI polymorphisms were found on lipid profile, lipoprotein (a) level, and quantitative CRP either in total population or in subgroups stratified by gender. In conclusion, our data demonstrate that ESR1 PvuII and XbaI gene polymorphisms did not seem to have an effect on lipoprotein metabolism or on inflammatory variables such as CRP.
authors.affiliation: Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran. maboroumand@yahoo.com
authors.forename: Mohammadali
authors.initials: M
authors.lastname: Boroumand
authors.forename: Mahboubeh
authors.initials: M
authors.lastname: Ghaedi
authors.forename: Narges
authors.initials: N
authors.lastname: Mohammadtaghvaei
authors.forename: Leila
authors.initials: L
authors.lastname: Pourgholi
authors.forename: Maryam Sotoudeh
authors.initials: MS
authors.lastname: Anvari
authors.forename: Gholamreza
authors.initials: G
authors.lastname: Davoodi
authors.forename: Alireza
authors.initials: A
authors.lastname: Amirzadegan
authors.forename: Soheil
authors.initials: S
authors.lastname: Saadat
authors.forename: Mahmood
authors.initials: M
authors.lastname: Sheikhfathollahi
authors.forename: Hamidreza
authors.initials: H
authors.lastname: Goodarzynejad
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood*; D003324:Coronary Artery Disease / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D047628:Estrogen Receptor alpha / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007492:Iran; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic
chemical_list: D015415:Biomarkers; D047628:Estrogen Receptor alpha; D008055:Lipids; D017270:Lipoprotein(a)