SMAD3 gene methylation profile and asthma in childhood: A longitudinal approach

Asthma is the most common chronic disease in childhood, and if not treated properly, may accelerate the loss of respiratory capacity in adulthood. Intrauterine and early postnatal exposures may play an important role in short- and long-term health outcomes. Epigenetic factors are associated with asthma development. DNA methylation of the SMAD3 (SMAD family member 3) promoter region is associated with asthma and can be influenced by genetic and environmental factors.

To evaluate the variation in the methylation profile of the SMAD3 promoter region in children from different intrauterine environments over time, a longitudinal observational study was conducted with 26 children. They were divided into three groups: children of smoking pregnant women (TBC) (n = 10), small-for-gestational-age due to idiopathic intrauterine growth restriction (IGR) (n = 06), and control group (CTR) (n = 10). Genomic DNA was obtained from epithelial mucosal cells at birth and at preschool age. The methylation profile was assessed by RT-PCR.

Although there were no differences in spirometry results or ISAAC questionnaire among the groups, a significant difference was observed in SMAD3 gene methylation between the TBC and IGR groups (p < 0·05) at birth. A difference was also observed in the rate of SMAD3 methylation in newborns exposed to smoking in the prenatal period and those born with IGR. This difference disappeared at the preschool age.

The impact of these results and their relationship with the evolution of children's health and the incidence of asthma in the long term remains to be clarified.