Regulation of Na,K-ATPase β1 mRNA content by thyroid hormone in neonatal rat cardiac myocytes

Incubation of primary cultures of neonatal rat cardiac myocytes in the presence of 100 nM triiodothyronine (T3) resulted in a three- to fivefold increase in the content of Na,K-ATPase β1 subunit mRNA which was maximal at 1 d of exposure to hormone. To investigate the mechanism by which T3 stimulates the abundance of β1 mRNA, transient transfection experiments were conducted with a chimeric gene containing a portion of the 5′ end of the rat β1 gene linked to a luciferase reporter gene. We found no effect of T3 on chimeric gene activity either in the absence or presence of cotransfected T3 receptor. The effect of T3 on the transcription rate of the endogenous β1 gene was quantitated by the nuclear run-on assay. T3 had no effect on β1 gene transcription following either 1 or 3 d of exposure and yielded a 1.3-fold increase at 6 d. These data indicate that T3 induction of Na,K-ATPase β1 mRNA content in neonatal rat cardiac myocytes in vitro is primarily mediated at a post-transcriptional site.