© 2001 American Heart Association, Inc.
Cellular Biology |
Thyroid Hormone Activation in Human Vascular Smooth Muscle Cells
Expression of Type II Iodothyronine Deiodinase
From the First Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Correspondence to Masami Murakami, MD, First Department of Internal Medicine, Gunma University School of Medicine, Maebashi 371-8511, Japan. E-mail mmurakam{at}showa.gunma-u.ac.jp
Abstract—Thyroid hormone has been reported to have significant effects on the peripheral vascular system, including relaxation of vascular smooth muscle cells and antiatherosclerotic effects. To exert its biological activity, thyroxine, which is a major secretory product of thyroid gland, needs to be converted to 3,5,3'-triiodothyronine (T3) by iodothyronine deiodinase. Type I iodothyronine deiodinase (DI) is widely distributed and maintains circulating T3 level, whereas type II iodothyronine deiodinase (DII) is present in a limited number of tissues to provide local intracellular T3. In the present study, we have identified iodothyronine deiodinase in cultured human coronary artery smooth muscle cells (hCASMCs) and human aortic smooth muscle cells (hASMCs). All of the characteristics of the deiodinating activity in hCASMCs and hASMCs were compatible with DII. Northern analysis demonstrated that DII mRNA was expressed in both hCASMCs and hASMCs, and DII mRNA levels as well as DII activities were rapidly increased by dibutyryl-cAMP or forskolin. These data demonstrate, for the first time, the expression of DII in human vascular smooth muscle cells, which is regulated by a cAMP-mediated mechanism. The present results suggest a previously unrecognized role of local T3 production by DII in the pathophysiology of human vascular smooth muscle cells.
Key Words: coronary artery smooth muscle • aortic smooth muscle • thyroid hormone receptor • cAMP
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