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Regulation of Rat Cardiac Kv1.5 Gene Expression by Thyroid Hormone Is Rapid and Chamber Specific¹

Division of Endocrinology, Department of Medicine, and Department of Pediatrics, North Shore University Hospital/New York University School of Medicine, Manhasset, New York 11030

Address all correspondence and requests for reprints to: Kaie Ojamaa, Ph.D., Division of Endocrinology, North Shore University Hospital, 300 Community Drive, Manhasset, New York 11030. E-mail: kojamaa{at}nshs.edu

Thyroid hormone affects the contractile and electrophysiological properties of the cardiac myocyte that result in part from changes in the expression of thyroid hormone-responsive cardiac genes, including those that regulate membrane ion currents. To determine the molecular mechanisms underlying this effect, expression of a voltage-gated K⁺ channel, Kv1.5, was measured in response to thyroid hormone. Using quantitative RT-PCR methodology, the content of Kv1.5 messenger RNA (mRNA) in left ventricles of euthyroid rats was 4.25 ± 0.6 x 10^-20 mol/µg total RNA and was decreased by 70% in the hypothyroid rat ventricle to 1.27 ± 0.80 x 10^-20 mol/µg RNA (P < 0.01). Administration of T₃ to hypothyroid animals restored ventricular Kv1.5 mRNA to control levels within 1 h of treatment, making this the most rapid T₃-responsive cardiac gene reported to date. The half-life of Kv1.5 mRNA was 1.9 h and 2.0 h in euthyroid and hypothyroid ventricles, respectively, and T₃ treatment of the rats did not alter its half-life. In atrial myocardium, expression of Kv1.5 mRNA (6.10 ± 0.37 x 10^-20 mol/µg RNA) was unaltered by thyroid hormone status. The myocyte-specific and chamber-selective expression of Kv1.5 mRNA was confirmed in primary cultures of rat atrial and ventricular myocytes.

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