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Increased deformability of red blood cells is associated with a deletion polymorphism of the angiotensin-converting enzyme gene

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dc.contributor.author Bor-Küçükatay, Melek
dc.contributor.author Turgut, S.
dc.contributor.author Emmungil, G.
dc.contributor.author Turgut, G.
dc.contributor.author Küçükatay, Vural
dc.date.accessioned 2019-08-16T11:36:11Z
dc.date.available 2019-08-16T11:36:11Z
dc.date.issued 2006
dc.identifier.issn 00408727 (ISSN)
dc.identifier.uri http://acikerisim.pau.edu.tr:8080/xmlui/handle/11499/4675
dc.description.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.
dc.language.iso English
dc.relation.isversionof 10.1620/tjem.208.147
dc.rights info:eu-repo/semantics/openAccess
dc.subject Angiotensin-converting enzyme
dc.subject Hemorheology
dc.subject Polymorphism
dc.subject angiotensin I
dc.subject angiotensin II
dc.subject bradykinin
dc.subject dipeptidyl carboxypeptidase
dc.subject adult
dc.subject allele
dc.subject article
dc.subject blood rheology
dc.subject blood vessel tone
dc.subject cardiovascular disease
dc.subject cardiovascular risk
dc.subject chromosome 17
dc.subject controlled study
dc.subject DNA polymorphism
dc.subject erythrocyte aggregation
dc.subject erythrocyte deformability
dc.subject female
dc.subject gene deletion
dc.subject gene insertion
dc.subject genetic association
dc.subject genotype
dc.subject high risk patient
dc.subject human
dc.subject intron
dc.subject male
dc.subject plasma viscosity
dc.subject prevalence
dc.subject renin angiotensin aldosterone system
dc.subject volunteer
dc.subject Adult
dc.subject Erythrocyte Deformability
dc.subject Female
dc.subject Gene Frequency
dc.subject Genotype
dc.subject Humans
dc.subject Male
dc.subject Peptidyl-Dipeptidase A
dc.subject Polymorphism, Genetic
dc.title Increased deformability of red blood cells is associated with a deletion polymorphism of the angiotensin-converting enzyme gene
dc.type Article
dc.relation.journal Tohoku Journal of Experimental Medicine
dc.contributor.authorID 0000-0002-6850-6281
dc.identifier.volume 208
dc.identifier.issue 2
dc.identifier.startpage 147
dc.identifier.endpage 155
dc.relation.publicationCategory Uluslararası Hakemli Dergi
dc.identifier.index Scopus
dc.identifier.index WOS
dc.identifier.index PubMed

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