DNA Methylation Pattern of CALCA and CALCB in Extremely Premature Infants with Monochorionic Triplets after Single‐Embryo Transfer

Abstract

Compared with full-term peers, premature infants are more likely to suffer from neonatal diseases and death. Variations in DNA methylation may affect these pathological processes. Calcitonin gene-related peptide (CGRP) plays a complex and diversified role in reproduction and chronic inflammation, and participates in the functional maintenance of vascular adaptation and trophoblast cells during pregnancy. Here, premature live births with single-chorionic triple embryos after single-embryo transfer were used as research objects, while full-term infants with double embryos and double-chorionic twins were used as controls. DNA was extracted from umbilical cord tissues for pyrosequencing to detect the methylation level of CpG island in CGRP promoter region. The average values of CGRP methylation in the umbilical cord tissues of very premature fetuses were higher than that of normal controls obtained from the databases. Immunofluorescence results showed that the expression of αCGRP was decreased in the blood vessel wall of the umbilical cord of monozygotic triplets, especially in death cases, while the βCGRP had a compensatory expression. In conclusion, our findings suggest that hypermethylation of CGRP might be considered as an important cause of serious neonatal morbidities.

Expression of mRNAs for DNA-methyltransferases and histone deacetylases in granulosa cells and follicular fluid of women undergoing in vitro fertilization: A pilot study

“…It is to be noted that variations of DNA methylation in samples from the placental and umbilical cord tissues, saliva and cord blood of new birth weight neonates have been claimed to mediate perinatal programming of non-communicable diseases later in life. Genome-wide DNA methylation studies have revealed association between differentially methylated DNA and neurodevelopmental impairments and compromised immune functions of the neonates [40][41][42][43].…”

Pathomechanisms of Prenatally Programmed Adult Diseases

“…It is also to be noted that variations of DNA methylation in samples from the placental and umbilical cord tissues, saliva, and cord blood of low-birthweight neonates have been claimed to mediate perinatal programming of several diseases later in life. Genome-wide methylation studies have revealed an association between differentially methylated DNA, neurodevelopmental impairments, and compromised immune functions in neonates [72][73][74][75].…”