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Association of Methylation Status of Promoter Region of Methylene Tetrahydrofolate Reductase Gene with Congenital Heart Disease

ZHANG Wen-di,YU Xiao,HUANG Shan,LUO Xiao-ping(Department of Pediatrics,Tongji Hospital Affiliated to Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,Hubei Province,China)  
Objective To compare the methylation status of the promoter region of methylene tetrahydrofolate reductase(MTHFR) gene in children with congenital heart disease(CHD) and control children without congenital birth defects,in order to explore the relationship between MTHFR promoter methylation status and CHD in children.Methods Peripheral venous blood samples of 53 patients with CHD(case group) and 80 control children without congenital birth defects(control group) were collected.All subjects were 10 months-14 years old,and were all from Wuhan city and its outskirts,29 cases were male and 24 cases were female in case group,and 44 cases were male and 36 cases were female in control group,and they were all Hans.The DNA from leukocytes was Abstracted.Then,the DNA was modified by sodium bisulfite and detected by methylation specific PCR(MSP) amplification;the primers were used to detect the methylation status in the promoter region of MTHFR.And the relationship of the methylation status of promoter region of MTHFR and CHD was analyzed by chi-square test using SPSS 15.0 software.Results The MSP analysis revealed that the numbers of non-complete methylation in the cases group and the control group were 36(67.92%) cases and 69(86.25%) cases,respectively;the numbers of partial methylation in case group and control group were 15(28.30%) cases and 9(11.25%) cases,respectively;the numbers of complete methylation in case group and control group were 2(3.78%) cases and 2(2.50%) cases respectively.There was a significantly statistical difference between the 2 groups(χ2=6.554,P=0.038).Conclusion The causative mechanisms of CHD is possibly correlative with the hypermethylation of the promoter region of MTHFR.
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