Foetal nicotine exposure causes PKCε gene repression by promoter methylation in rat hearts.

ABSTRACT:

Aims

foetal nicotine exposure results in decreased protein kinase C epsilon (PKCε) expression and increased cardiac vulnerability to ischaemia and reperfusion injury in adult rat offspring. The present study tested the hypothesis that maternal nicotine administration causes increased promoter methylation of the PKCε gene resulting in PKCε repression in the heart.

Methods and results

nicotine treatment of pregnant rats starting at day 4 of gestation increased the methylation of the Egr-1 binding site at the PKCε gene promoter and decreased PKCε protein and mRNA abundance in near-term foetal hearts. Methylation of the Egr-1 binding site reduced Egr-1 binding to the PKCε promoter in the heart. Site-specific deletion of the Egr-1 binding site significantly decreased PKCε promote

SUBMITTER: Lawrence J 

PROVIDER: S-EPMC3002869 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature