Abstract：OBJECTIVE: To study the role of promoter methylation of insulin-like growth factor binding protein 3 (IGFBP3) in intrauterine growth restriction (IUGR). METHODS: Fifty neonates with IUGR and 30 healthy neonates were enrolled. The promoter methylation status of IGFBP3 in peripheral blood was evaluated by methylation-specific PCR (MSP) and high resolution melting (HRM) techniques. RESULTS: The complete methylation rate, partial methylation rate and non-methylation rate of IGFBP3 promoter in the IUGR group was 4% (2/50), 40% (20/50) and 56% (28/50), respectively. The partial methylation rate and non-methylation rate of IGFBP3 promoter in the control group were 13% (4/30) and 87% (26/30), respectively. There were significant differences in the promoter methylation rate of IGFBP3 between the two groups (P<0.01). CONCLUSIONS: The promoter methylation of IGFBP3 gene is associated with the pathogenesis of IUGR.
SU Ai-Ling,JIANG Li,GE Qin-Yu. Methylation of insulin-like growth factor binding protein 3 gene in neonates with intrauterine growth restriction[J]. CJCP, 2011, 13(9): 700-703.
［1］Mamelle N, Bonid M, Rivière O, Joly MO, Mellier G, Maria B, et al. Identification of newborns with fetal growth restriction (FGR)in weight and/or length based on constitutional growth potential［J］. Eur J Pediatr, 2006, 165(10): 717-725.
［2］Bos AF, Einspieler C, Prechtl HF. Intrauterine growth retardation, general movements, and neurodevelopmental outcome: a review［J］. Dev Med Child Neurol, 2001,43(1):61-68.
［6］Lorente A, Mueller W, Urdangarín E, L-zcoz P, von Deimling A, Castresana JS. Detection of methylation in promoter seguences by melting curve analysis-based semiguantitative real time PCR［J］. BMC Cancer, 2008, 8: 61.
［7］Turner CL, Mackay DM, Callaway JL, Docherty LE, Poole RL, Bullman H, et al. Methylation analysis of 79 patients with growth restriction reveals novel patterns of methylation change at imprinted loci［J］. Eur J Hum Genet, 2010, 18(6):648-655.
［8］Paquette J, Bessette B, Ledru E, Deal C. Identification of upstream stimulatory factor binding sites in the human IGFBP3 promoter and potential implication of adjacent singlenucleotide polymorphisms and responsiveness to insulin［J］. Endocrinology, 2007, 148(12):6007-6018.
［9］Kawasaki T, Nosho K, Ohnishi M, Suemoto Y, Kirkner GJ, Fuchs CS, et al. IGFBP3 promoter methylation in colorectal cancer: relationship with microsatellite instability, CpG island methylator phenotype, and p53［J］. Neoplasia, 2007, 9(12): 1091-1098.
［10］Dolinoy DC, Huang D, Jirtle RL. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development［J］. Proc Natl Acad Sci U S A, 2007, 104(32):13056-13061.
［11］Lillycrop KA, Phillips ES, Jackson AA, Hanson MA, Burdge GC. Dietary protein restriction of pregnant rats induces and folic acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring［J］. J Nutr, 2005,135(6):1382-1386.
［12］Torrens C, Brawley L, Anthony FW, Dance CS, Dunn R, Jackson AA, et al. Folate supplementation during pregnancy improves offspring cardiovascular dysfunction induced by protein restriction［J］. Hypertension, 2006, 47(5): 982-987.
