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*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*LIOTHYRONINE
Endocrinology Vol. 140, No. 7 3170-3176
Copyright © 1999 by The Endocrine Society

ARTICLES

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

Kaie Ojamaa, Amin Sabet, Agnes Kenessey, Rajesh Shenoy and Irwin Klein

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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