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[The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease].
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2005 Apr; 22(2):164-8.ZY

Abstract

OBJECTIVE

To investigate associations between the apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease (CAD).

METHODS

apoE genotypes were identified by multiplex amplification refractory mutation system (multi-ARMS) and the polymorphisms of both apoCI and apoCII genes were detected by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 203 cases of CAD and 365 controls. Pairwise linkage disequilibrium coefficients (D, D') were estimated by the LINKAGE program.

RESULTS

The frequencies of apoE E3/4 genotype (0.259) and epsilon4 (0.139) in CAD group were significantly higher than that in control group (0.125, 0.069), (P<0.05). The significant difference was also found for the apoCI locus, the frequencies of H2 allele were 0. 205 in the CAD and 0.113 in the control. Linkage disequilibrium coefficient D' was 0.672 (P<0.01) between apoE and apoCI genes. Significant differences for a deficit of epsilon3-H1-T1 and excess of epsilon4-H2-T1 were found in the CAD by estimation of the haplotype frequencies. After adjustment for possible confounding factors, the multivariate Logistic analysis showed a significant interaction among epsilon4, H2 and smoking, OR value was 18.3 (95%CI:2.35-150.81, P<0.05), attributable proportions of interaction (API) was 57.3%, it was a multiplicative model. An additive model was shown among epsilon4, H2 and bibulosity; the odds ratio (OR) (95%CI) and API of their interaction were 12.7(2.8-58.6, P<0.05) and 43.5%, respectively.

CONCLUSION

The results suggested that both apoE and apoCI on chromosome 19 were the susceptibility loci for CAD, their linkage disequilibrium should be responsible for the development of CAD. Smoking and bibulosity can significantly increase the risk of CAD.

Authors+Show Affiliations

Department of Hygiene, School of Medicine, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071 P. R. China. chwang027@yahoo.com.cnNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

15793777

Citation

Wang, Chunhong, et al. "[The Apolipoprotein E-CI-CII Gene Cluster Polymorphisms and Coronary Artery Disease]." Zhonghua Yi Xue Yi Chuan Xue Za Zhi = Zhonghua Yixue Yichuanxue Zazhi = Chinese Journal of Medical Genetics, vol. 22, no. 2, 2005, pp. 164-8.
Wang C, Zhou X, Zheng F, et al. [The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2005;22(2):164-8.
Wang, C., Zhou, X., Zheng, F., Han, D., Shi, Q., & Liu, F. (2005). [The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi = Zhonghua Yixue Yichuanxue Zazhi = Chinese Journal of Medical Genetics, 22(2), 164-8.
Wang C, et al. [The Apolipoprotein E-CI-CII Gene Cluster Polymorphisms and Coronary Artery Disease]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2005;22(2):164-8. PubMed PMID: 15793777.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [The apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease]. AU - Wang,Chunhong, AU - Zhou,Xin, AU - Zheng,Fang, AU - Han,Dingfen, AU - Shi,Qun, AU - Liu,Fang, PY - 2005/3/29/pubmed PY - 2009/4/3/medline PY - 2005/3/29/entrez SP - 164 EP - 8 JF - Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics JO - Zhonghua Yi Xue Yi Chuan Xue Za Zhi VL - 22 IS - 2 N2 - OBJECTIVE: To investigate associations between the apolipoprotein E-CI-CII gene cluster polymorphisms and coronary artery disease (CAD). METHODS: apoE genotypes were identified by multiplex amplification refractory mutation system (multi-ARMS) and the polymorphisms of both apoCI and apoCII genes were detected by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 203 cases of CAD and 365 controls. Pairwise linkage disequilibrium coefficients (D, D') were estimated by the LINKAGE program. RESULTS: The frequencies of apoE E3/4 genotype (0.259) and epsilon4 (0.139) in CAD group were significantly higher than that in control group (0.125, 0.069), (P<0.05). The significant difference was also found for the apoCI locus, the frequencies of H2 allele were 0. 205 in the CAD and 0.113 in the control. Linkage disequilibrium coefficient D' was 0.672 (P<0.01) between apoE and apoCI genes. Significant differences for a deficit of epsilon3-H1-T1 and excess of epsilon4-H2-T1 were found in the CAD by estimation of the haplotype frequencies. After adjustment for possible confounding factors, the multivariate Logistic analysis showed a significant interaction among epsilon4, H2 and smoking, OR value was 18.3 (95%CI:2.35-150.81, P<0.05), attributable proportions of interaction (API) was 57.3%, it was a multiplicative model. An additive model was shown among epsilon4, H2 and bibulosity; the odds ratio (OR) (95%CI) and API of their interaction were 12.7(2.8-58.6, P<0.05) and 43.5%, respectively. CONCLUSION: The results suggested that both apoE and apoCI on chromosome 19 were the susceptibility loci for CAD, their linkage disequilibrium should be responsible for the development of CAD. Smoking and bibulosity can significantly increase the risk of CAD. SN - 1003-9406 UR - https://www.unboundmedicine.com/medline/citation/15793777/[The_apolipoprotein_E_CI_CII_gene_cluster_polymorphisms_and_coronary_artery_disease]_ L2 - https://medlineplus.gov/coronaryarterydisease.html DB - PRIME DP - Unbound Medicine ER -