Research Article

Variants -250G/A and -514C/T in the LIPC gene are associated with hypertensive disorders of pregnancy in Chinese women

Published: August 07, 2014
Genet. Mol. Res. 13 (3) : 6126-6134 DOI: 10.4238/2014.August.7.28

Abstract

We examined the influence of the promoter polymorphisms -250G/A (rs2070895) and -514C/T (rs1800588) in the human hepatic lipase (LIPC) gene on dyslipidemia and hypertensive disorders complicating pregnancy (HDCP) in a Chinese population. Clinically defined HDCP patients (N = 321) and healthy pregnant women (N = 331) were recruited and genotyped using polymerase chain reaction-restriction fragment length polymorphism for the two LIPC single nucleotide polymorphisms (SNPs). The results showed significant relationships between HDCP and triglycerides, apolipoprotein A1, and high-density lipoprotein cholesterol (P ≤ 0.004), although no significant association was found between HDCP and LIPC genotypes or alleles. Significant linkage disequilibrium of the two SNPs was found in both HDCP patients (R2 = 0.867) and controls (R2 = 0.91). Body mass index (BMI) was associated with -250G/A in women with mild preeclampsia (MPE) (P = 0.01). Carriers of the mutant homozygote -250AA genotype presented higher BMI in the MPE group. In conclusion, the LIPC -250G/A and -514C/T variants influenced TC and SBP levels in GH patients and the BMI level in the MPE group, although there was no evidence to validate an association between HDCP and LIPC allele, genotype, or haplotype frequencies.

We examined the influence of the promoter polymorphisms -250G/A (rs2070895) and -514C/T (rs1800588) in the human hepatic lipase (LIPC) gene on dyslipidemia and hypertensive disorders complicating pregnancy (HDCP) in a Chinese population. Clinically defined HDCP patients (N = 321) and healthy pregnant women (N = 331) were recruited and genotyped using polymerase chain reaction-restriction fragment length polymorphism for the two LIPC single nucleotide polymorphisms (SNPs). The results showed significant relationships between HDCP and triglycerides, apolipoprotein A1, and high-density lipoprotein cholesterol (P ≤ 0.004), although no significant association was found between HDCP and LIPC genotypes or alleles. Significant linkage disequilibrium of the two SNPs was found in both HDCP patients (R2 = 0.867) and controls (R2 = 0.91). Body mass index (BMI) was associated with -250G/A in women with mild preeclampsia (MPE) (P = 0.01). Carriers of the mutant homozygote -250AA genotype presented higher BMI in the MPE group. In conclusion, the LIPC -250G/A and -514C/T variants influenced TC and SBP levels in GH patients and the BMI level in the MPE group, although there was no evidence to validate an association between HDCP and LIPC allele, genotype, or haplotype frequencies.