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VANADIUM EXPOSURE ALTERS SPONTANEOUS BEAT RATE AND GENE EXPRESSION OF CULTURED CARDIAC MYOCYTES
Citation:
Devlin, R B., D. Graff, L. A. Dailey, AND W. Cascio. VANADIUM EXPOSURE ALTERS SPONTANEOUS BEAT RATE AND GENE EXPRESSION OF CULTURED CARDIAC MYOCYTES. Presented at Society of Toxicology, Baltimore, MD, March 21-25, 2004.
Description:
Ambient air pollution particulate matter (PM) exposure is associated with increased morbidity and mortality. Recent toxicological studies report PM-induced changes in a number of cardiac parameters, including heart rate variability, arrhythmias, repolarization, and internal defibrillator discharges. In this study we identify cellular processes that might contribute to cardiac dysfunction after PM exposure. Isolated neonatal rat ventricular myocytes were cultured for 11 days and then exposed to different concentrations of vanadium (V), a common soluble PM component. A 30 min exposure to V decreased spontaneous myocyte beat rate by 10% compared to baseline, an effect that persisted at 1, 2, 4, and 24 hrs. To account for this decrease in beat rate, we used real-time PCR to test for changes in gene expression of several ion channels that contribute to repolarization, gap junction proteins (mediators of intercellular communication), and markers of inflammation following 6 and 24 hrs of V exposure. A 6 hr exposure did not affect connexin or ion channel gene expression but increased expression of IL-6, IL-1a, and HSP70 1.5-2-fold. A 24 hr exposure produced 1.5-2-fold increases in gene expression of the gap junction protein connexin 43, IL-6, and IL-1a, and a 50% decrease in the K+ channel coded for by the gene KvLQt1. These data suggest that soluble metals found in air pollution particles could contribute to PM-associated cardiac morbidity and mortality by affecting the function of cardiac myocytes. These effects may be triggered by an inflammatory response or by the remodeling of proteins associated with cellular communication and/or repolarization. This abstract does not necessarily reflect EPA policy.