Imprinted Genes PEG1 And PEG3 MRNA Expression And Promoter Methylation In The Human Abnormal Birth Weight Placenta

ObjectiveIn this study, we performed a systematic survey of the variation of the imprinted gene Paternally expressed 1 (PEG1) and Paternally expressed gene 3 (PEG3) expression and promoter methylation status in the human abnormal birth weight placentae without any pregnancy-related complications.MethodIn the placenta with high birth weight(birth weight≥4000g), normal birth weight(2500g≤birth weight<4000g) and low birth weight(birth weight<2500g), we have evaluated PEG1 and PEG3 expression levels with real-time reverse-transcriptase polymerase chain reaction (PCR) analysis. Promoter methylation was measured by the bisulfite genomic sequencing method.Results(1) Imprinted gene PEG1 and PEG3 expression:high birth weight(11.66±9.01 and 16.45±10.13), low birth weight(0.84±0.49 and 0.85±0.67) and normal birth weight(1.10±0.77 and 1.11±0.60). Both genes were significantly up-regulated in high birth weight compared to normal birth weight (P<0.05), and there were no significant difference between normal birth weight and low birth weight(P>0.05) about the two genes.(2) PEG1 promoter methylation:high birth weight(0.497±0.023), low birth weight(0.502±0.021) and normal birth weight(0.503±0.019), the level among three groups keep stable(P>0.05). PEG3 promoter methlation:high birth weight(0.131±0.027), low birth weight(0.167±0.035) and normal birth weight(0.162±0.018), the level was down-regulated in high birth weight compared with normal birth weight, but the methylation between low birth weight and normal birth weight was no significant change.(3) We discovered up-regulated expression of PEG3 was accompanied by down-regulated DNA methylation level within objective fragment of promoter region (R=-0.845; P＜0.01).ConclusionThis study showed the two genes up-regulated expression may be a cause of human high birth weight. The reduction of methylation pattern in the promoter region of PEG3 may up-regulate expression and contribute to the mechanism of human high birth weight.