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Published on: September 17, 2014
CD36 genotype associated with ischemic stroke in Chinese Han
Yong Zhang1, Jing Zang2, Bin Wang3
1Department of Neurology, Jinan Central Hospital, Shandong University Shandong, P. R. China.
Insights
Specific CD36 gene variations (SNPs) are linked to an increased risk of ischemic stroke. These findings highlight CD36 as a potential genetic marker for stroke susceptibility in the Chinese Han population.
Area of Science:
- Genetics
- Cardiovascular Medicine
- Neurology
Background:
- CD36 plays a role in oxidant stress, hyperlipidemia, and thrombosis, key factors in stroke pathology.
- CD36 single nucleotide polymorphisms (SNPs) are associated with metabolic abnormalities and increased risk for cardiovascular diseases.
- These associations suggest CD36 as a candidate gene for stroke.
Purpose of the Study:
- To investigate the association between CD36 SNPs and ischemic stroke risk.
- To explore the genetic susceptibility to stroke conferred by CD36.
Main Methods:
- A case-control study involving 374 atherothrombotic stroke patients and 1,013 controls.
- Genotyping of five CD36 SNPs (rs3211842, rs3211870, rs1761667, rs9784998, rs10499859) using PCR-ligase detection reaction.
- Logistic regression analysis was employed to assess risk, adjusting for covariates.
Main Results:
- SNPs rs1761667 and rs10499859 showed a significant association with ischemic stroke.
- Carriers of rs1761667 (A allele) had a 1.38-fold increased risk (adjusted odds ratio).
- Carriers of rs10499859 (G allele) had a 1.39-fold increased risk (adjusted odds ratio).
- The studied SNPs were in strong linkage disequilibrium and showed no association with plasma lipid levels or thromboxane B2 expression.
Conclusions:
- CD36 SNPs, specifically rs1761667 and rs10499859, may contribute to genetic susceptibility to ischemic stroke.
- These findings suggest a potential role for CD36 in the genetic predisposition to stroke among the Chinese Han population.
Objective:
CD36 is involved in oxidant stress, hyperlipidemia, and thrombosis in the pathology of stroke. CD 36 single nucleotide polymorphisms (SNPs) were reported to be associated with abnormalities of serum FA, triglyceride level and to increase risk of metabolic syndrome, coronary artery disease and type 2 diabetes. Based on these finding we hypothesized that CD36 is an important candidate gene of stroke; therefore, we set out a case-control study to explore the association of CD36 SNPs with ischemic stroke.
Methods:
We enrolled 374 patients with atherothrombotic stroke as cases and 1,013 people without stroke as controls. CD36 rs3211842, rs3211870, rs1761667, rs9784998, and rs10499859 loci were detected by PCR-ligase detection reaction.
Results:
Only rs1761667 (P=0.042) and rs10499859 (P=0.038) polymorphisms were associated with cases of ischemic stroke. Under a dominant genetic model, logistic regression analysis revealed a 1.34-fold increased risk (95% CI 1.05-1.72) of ischemic stroke with rs1761667 A than non-A carriers (P=0.020); the adjusted odds ratio (AOR) was 1.38 (95% CI 1.06-1.78) after adjusting for the covariates age, gender, body mass index (BMI), cigarette smoking, hypertension, and diabetes. For rs10499859, the risk was increased 1.36-fold for G than non-G carriers (P=0.016), and the AOR was 1.39 (95% CI 1.08-1.81) (P=0.012). The 5 SNPs were in strong linkage disequilibrium. CD36 SNPs may have no association with plasma lipid levels and thromboxane B2 (TXB2) expression.
Conclusion:
CD36 rs1761667 and rs10499859 may indicate genetic susceptibility to ischemic stroke among Chinese Han.
