CDKN2B Methylation and Aortic Arch Calcification in Patients with Ischemic Stroke.
J Atheroscler Thromb
; 24(6): 609-620, 2017 Jun 01.
Article
em En
| MEDLINE
| ID: mdl-27773886
ABSTRACT
AIM:
CDKN2A/2B near chromosome 9p21 has been proposed as a potential genetic etiology for both atherosclerosis and arterial calcification. DNA methylation, which can change the expression of CDKN2A/2B, may be an underlying mechanism for this association. This study aimed to evaluate whether CDKN2A/2B methylation is related to aortic arch calcification (AAC) in patients with ischemic stroke.METHODS:
DNA methylation levels of CDKN2A/2B was measured using venous blood samples in 322 patients with ischemic stroke. A total of 36 CpG sites around promoter regions of CDKN2A/2B were examined. AAC was quantified with Agatston score based on results of computed tomography angiography.RESULTS:
There were 248 (77.0%) patients with and 74 (23.0%) patients without evident AAC. Compared with patients without AAC, patients with AAC had higher methylation levels of CDKN2B (5.72 vs 4.94, Pï¼0.001). Using a generalized linear model, positive correlation between methylation levels and log-transformed calcification scores was detected at CDKN2B (ß=0.275±0.116, P= 0.018).CONCLUSION:
Patients with higher levels of DNA methylation of CDKN2B may bear increased risk for AAC. Further studies to reveal the underlying mechanisms of this association are warranted for establishing a cause-effect relationship.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Aorta Torácica
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Calcinose
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Acidente Vascular Cerebral
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Inibidor de Quinase Dependente de Ciclina p15
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Calcificação Vascular
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article