Gene expression profiling of DEHP-treated cardiomyocytes reveals potential causes of phthalate arrhythmogenicity.

ABSTRACT:

Background

Di-(2-ethylhexyl)-phthalate (DEHP) is a widely used plasticizer that imparts flexibility to polyvinyl chloride. We have recently reported that clinically relevant concentrations of DEHP can affect electrical coupling between cardiac myocytes causing significant rhythm disturbances. The underlying causes for this effect are currently unknown.

Objectives

To use data on global mRNA expression as a tool to reveal possible pathways leading to arrhythmogenic effects of DEHP.

Methods

Rat neonatal cardiomyocytes were treated with 50 μg/mL DEHP for 72 h. Extracted RNA samples were hybridized onto Affymetrix Rat Gene 1.0 ST arrays. The mRNA expression of a subset of genes was validated by qRT-PCR. In a second set of experiments, cells were treated in a concentration

SUBMITTER: Posnack NG 

PROVIDER: S-EPMC3003946 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature