Meeting Abstract
P2-6 - Treatment of chick embryos with thyroid hormone does not increase heart rate through increased heart mass, up-regulation of hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels, or upregulation of &beta1 receptors (&beta1 AR). Mark, PP*; Cunningham, BJ; Pirtle, TJ; The College of Idaho patrick.mark@yotes.collegeofidaho.edu
Thyroid hormone is a vital hormone in embryonic development. Elevated and depressed concentrations of thyroid hormone trigger the embryo to enter different phases throughout gestation. Pregnant women with thyroid issues can be dangerous for the embryo. We are studying the pathways and mechanisms that thyroid hormone uses to impact cardiac development. Our model organism is the chick embryo, and we treat embryos with thyroid hormone (1 nanomolar and 10 nanomolar) and observe their impact on cardiac development. Our hypothesis is that thyroid hormone increases heartrate either through the upregulation of hyperpolarized-activated cyclic nucleotide-gated cation (HCN) channels, increased heart mass, or upregulation of &beta1 adrenergic receptors (&beta1 AR). Our experiments include electrocardiograms in ovo to measure heartrate, pharmacological experiments with isolated perfused hearts to identify &beta1 AR upregulation, heart dissections to measure heart mass, and ELISA kits for HCN channel upregulation measurements. Our data suggests that there is a statistically significant difference in heartrate from thyroid hormone treated embryos compared to the control. However, there is not a statistically significant difference in the heart mass, or HCN concentration, or &beta1 AR concentration compared to the controls. Therefore, we reject our hypothesis. We do not believe that the mechanisms that thyroid hormone uses to increase heartrate are through the upregulation of the HCN channel, through increased heart mass, or upregulation of &beta1 AR.