TY - JOUR
T1 - Polymorphism in maternal LRP8 gene is associated with fetal growth
AU - Wang, Lin
AU - Wang, Xiaobin
AU - Laird, Nan
AU - Zuckerman, Barry
AU - Stubblefield, Philip
AU - Xu, Xin
N1 - Funding Information:
This study was supported in part by grants 20-FY98-0701 and 20-FY02-56 from the March of Dimes Birth Defects Foundation, grant R01 HD41702 from the National Institute of Child Health and Human Development, and grants R01ES11682, R21 ES11666, and ES-00002 from the National Institute of Environmental Health Sciences. We thank the Boston University Medical Center preterm study advisory group and Drs. Paul Wise, Howard Bauchner, Jerome Klein, Milton Ketochuck, and John Katznica, for their support and guidance throughout the study. We thank Colleen Pearson, Katherine Ortiz, and Emault Louis for their effort in field data collection. We thank the nursing staff of Labor and Delivery at the Boston Medical Center for their assistance with our study. We thank Ann Ramsey, for administrative support, and Lingling Fu, for data entry and management.
PY - 2006/5
Y1 - 2006/5
N2 - Fetal growth restriction (FGR) affects >200,000 pregnancies in the United States annually and is associated with increased perinatal mortality and morbidity, as well as poorer long-term health for infants with FGR compared with infants without FGR. FGR appears to be a complex trait, but the role of genetic factors in the development of FGR is largely unknown. We conducted a candidate-gene association study of birth weight and FGR in two independent study samples obtained at the Boston Medical Center. We first investigated the association between maternal genotypes of 68 single-nucleotide polymorphisms (SNPs) from 41 candidate genes and fetal growth in a sample of 204 black women selected for a previous study of preeclampsia, 92 of whom had preeclampsia (characterized by high blood pressure and the presence of protein in the urine). We found significant association between SNP rs2297660 in the LRP8 gene and birth weight. Subsequently, we replicated the association in a larger independent sample of 1,094 black women; similar association between LRP8 and FGR was observed in this sample. The "A" allele at rs2297660 was associated with a higher standardized birth weight and a lower risk of FGR. Under the additive genetic model, each additional copy of the "A" allele reduced the risk of FGR by 33% (P < .05). In conclusion, results from the two independent samples of black women provide consistent evidence that SNP rs2297660 in LRP8 is associated with fetal growth.
AB - Fetal growth restriction (FGR) affects >200,000 pregnancies in the United States annually and is associated with increased perinatal mortality and morbidity, as well as poorer long-term health for infants with FGR compared with infants without FGR. FGR appears to be a complex trait, but the role of genetic factors in the development of FGR is largely unknown. We conducted a candidate-gene association study of birth weight and FGR in two independent study samples obtained at the Boston Medical Center. We first investigated the association between maternal genotypes of 68 single-nucleotide polymorphisms (SNPs) from 41 candidate genes and fetal growth in a sample of 204 black women selected for a previous study of preeclampsia, 92 of whom had preeclampsia (characterized by high blood pressure and the presence of protein in the urine). We found significant association between SNP rs2297660 in the LRP8 gene and birth weight. Subsequently, we replicated the association in a larger independent sample of 1,094 black women; similar association between LRP8 and FGR was observed in this sample. The "A" allele at rs2297660 was associated with a higher standardized birth weight and a lower risk of FGR. Under the additive genetic model, each additional copy of the "A" allele reduced the risk of FGR by 33% (P < .05). In conclusion, results from the two independent samples of black women provide consistent evidence that SNP rs2297660 in LRP8 is associated with fetal growth.
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U2 - 10.1086/503712
DO - 10.1086/503712
M3 - Article
C2 - 16642433
AN - SCOPUS:33646055822
SN - 0002-9297
VL - 78
SP - 770
EP - 777
JO - American journal of human genetics
JF - American journal of human genetics
IS - 5
ER -