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CDKN2B Methylation and Aortic Arch Calcification in Patients with Ischemic Stroke
Shuyu Zhou1, Biyang Cai1, Zhizhong Zhang1
1Department of Neurology, Jinling Hospital, Medical School of Nanjing University.
Journal of Atherosclerosis and Thrombosis
|October 25, 2016
Summary
Higher DNA methylation of CDKN2B is linked to aortic arch calcification (AAC) in ischemic stroke patients. This suggests CDKN2B methylation may increase the risk of arterial calcification.
Area of Science:
- Genetics
- Cardiovascular Disease
- Epigenetics
Background:
- The CDKN2A/2B gene locus at chromosome 9p21 is implicated in atherosclerosis and arterial calcification.
- DNA methylation of CDKN2A/2B may mediate this association by altering gene expression.
Purpose of the Study:
- To investigate the relationship between CDKN2A/2B DNA methylation and aortic arch calcification (AAC) in patients with ischemic stroke.
Main Methods:
- DNA methylation levels of CDKN2A/2B were analyzed in blood samples from 322 ischemic stroke patients.
- 36 CpG sites in the promoter regions of CDKN2A/2B were examined.
- Aortic arch calcification (AAC) was quantified using Agatston scores from computed tomography angiography.
Main Results:
- Aortic arch calcification (AAC) was present in 77.0% of patients.
- Patients with AAC exhibited significantly higher CDKN2B methylation levels compared to those without AAC (5.72 vs. 4.94, P < 0.001).
- A positive correlation was found between CDKN2B methylation levels and AAC severity (β=0.275±0.116, P=0.018).
Conclusions:
- Elevated DNA methylation of CDKN2B is associated with an increased risk of aortic arch calcification (AAC).
- Further research is needed to elucidate the causal mechanisms linking CDKN2B methylation and AAC.
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