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Acta Physiologica 2010; Volume 198, Supplement 677
Joint Meeting of the Scandinavian and German Physiological Societies
3/27/2010-3/30/2010
Copenhagen, Denmark
HYPOTHYROIDISM OF GENE TARGETED MICE LACKING KCNQ1
Abstract number: P-MON-55
FROHLICH1 H, BOINI1 KM, SEEBOHM1 G, STRUTZ-SEEBOHM1 N, URECHE1 O, FOLLER1 M, PFEIFER1 K, LANG1 F
Aims: Thyroid hormones T3/T4 participate in the fine tuning of development and performance. The function and growth of thyroids depends on K+ channels establishing the electrochemical gradient across the cell membrane. The present paper explored whether KCNQ1, a widely expressed voltage gated K+ channel, participates in the regulation of thyroid function. Methods: KCNQ1 transcript and protein abundance have been determined utilizing RT-PCR and confocal immunohistochemistry. Thyroid function has been analyzed in KCNQ1 deficient mice (kcnq1-/-) and their wild type littermates (kcnq1+/+). Results: KCNQ1 transcripts were abundant in thyroid gland tissue and KCNQ1 protein is expressed in follicular cells of the thyroid gland. Despite a tendency of TSH plasma concentrations to be higher in kcnq1-/- than in kcnq1+/+ mice, the thyroid mass, T3 and T4 plasma concentrations were significantly lower in kcnq1-/- than in kcnq1+/+ mice. Moreover, body temperature was significantly higher in kcnq1-/- than in kcnq1+/+ mice. In conclusion, KCNQ1 is required for proper function of thyroid glands.
To cite this abstract, please use the following information:
Acta Physiologica 2010; Volume 198, Supplement 677 :P-MON-55