Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/4675
Title: Increased deformability of red blood cells is associated with a deletion polymorphism of the angiotensin-converting enzyme gene
Authors: Bor-Küçükatay, Melek
Turgut, S.
Emmungil, G.
Turgut, G.
Küçükatay, Vural
Keywords: Angiotensin-converting enzyme
Hemorheology
Polymorphism
angiotensin I
angiotensin II
bradykinin
dipeptidyl carboxypeptidase
adult
allele
article
blood rheology
blood vessel tone
cardiovascular disease
cardiovascular risk
chromosome 17
controlled study
DNA polymorphism
erythrocyte aggregation
erythrocyte deformability
female
gene deletion
gene insertion
genetic association
genotype
high risk patient
human
intron
male
plasma viscosity
prevalence
renin angiotensin aldosterone system
volunteer
Adult
Erythrocyte Deformability
Female
Gene Frequency
Genotype
Humans
Male
Peptidyl-Dipeptidase A
Polymorphism, Genetic
Abstract: Angiotensin-converting enzyme (ACE) plays important roles in the renin-angiotensin system. ACE converts angiotensin I to angiotensin II and also inactivates bradykinin, thereby modulating the vascular tone. A polymorphism of the ACE gene, located on chromosome 17, has been found in intron 16, and is characterized by the presence (insertion [I]) or absence (deletion [D]) of a 287-base-pair Alu repeat. Individuals with the D allele of the ACE gene have higher ACE levels and are at higher risk of cardiovascular events. We aimed to investigate the possible relationship between the I/D polymorphism of the ACE gene and hemorheological parameters, including red blood cell (RBC) deformability. The study was performed on 28 healthy young volunteers (13 women and 15 men, mean age 24 ± 2). The prevalence of the I and D alleles was 30.4% and 69.6%, respectively. The I/I genotype (II) was found in 21.4%, I/D genotype (ID) in 17.9%, and D/D genotype (DD) in 60.7% of the subjects tested. No significant relationship between ACE I/D polymorphism and RBC aggregation or whole blood and plasma viscosity was observed. In contrast, RBC deformability was significantly increased in the subjects with the DD genotype compared with the II (p < 0.05) or the ID (p < 0.01) genotype, and in the subjects with the D allele compared with the I allele (p < 0.01). We suggest that RBC deformability of individuals with the D allele, who have higher risk for cardiovascular pathologies, may have been increased by a compensatory mechanism. © 2006 Tohoku University Medical Press.
URI: https://hdl.handle.net/11499/4675
https://doi.org/10.1620/tjem.208.147
ISSN: 0040-8727
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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