Does gene expression profiling of DEHP-treated cardiomyocytes reveal potential causes of phthalate arrhythmogenicity?
Exposure of neonatal rat cardiomyocytes to clinically relevant DEHP concentrations leads to global changes in mRNA expression. These changes help to explain the arrhythmogenic effects of phthalates on these cells.
The C allele of the A-444C polymorphism is a risk factor for AIU in our population and could be a genetic marker for this phenotype. Furthermore, this single-nucleotide polymorphism is mainly associated with the cutaneous clinical pattern and with low skin response to histamine.