title: Expression and regulation of type 2 iodothyronine deiodinase in rat aorta media.
abstract: Here, we have found that type 2 iodothyronine deiodinase (D2) is present in rat aorta media and that there is a circadian variation in the D2 expression. The D2 mRNA was approximately 4-fold higher at 0900 h than at 2100 h, and the activity was approximately 6-fold higher at noon than at 2100 h. The increase in aorta media D2 activity is preceded by the increase in its mRNA. The increase in D2 mRNA and activity in the circadian variation was reduced by the administration of prazosin, an alpha1-adrenergic antagonist, and propranolol, a beta- adrenergic antagonist. Furthermore, phenylephrine, an alpha1-adrenergic agonist, and isoproterenol, a beta-adrenergic agonist, caused a significant increase in D2 mRNA and activity. In the hypothyroid rats, aorta mediae D2 mRNA at both 0900 and 2100 h were not significantly different when compared with those in the euthyroid rats. On the other hand, aorta mediae D2 activity at both 1200 and 2100 h in the hypothyroid rats were approximately 2-fold higher. From these results, we suggest that D2 activity of rat aorta media is increased by both alpha1- and beta-adrenergic stimulation, at least partly, at the pretranslational level. We also suggest that both alpha1- and beta-adrenergic mechanisms may be involved, at least partly, in the circadian variation of the activity. In the hypothyroid state, the aorta media D2 activity is increased mainly by the posttranslational mechanism, and the similar circadian variation of the D2 expression is present as in the euthyroid state.
authors.affiliation: Department of Medicine II, Kansai Medical University, Moriguchi-City, Osaka 570, Japan.
authors.forename: Saori
authors.initials: S
authors.lastname: Yasuzawa-Amano
authors.forename: Nagaoki
authors.initials: N
authors.lastname: Toyoda
authors.forename: Akimasa
authors.initials: A
authors.lastname: Maeda
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kosaki
authors.forename: Yasukiyo
authors.initials: Y
authors.lastname: Mori
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
authors.forename: Mitsushige
authors.initials: M
authors.lastname: Nishikawa
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000201:enzymology*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D007037:Hypothyroidism / Q000503:physiopathology*; D007453:Iodide Peroxidase / Q000235:genetics*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D017540:Tunica Media / Q000201:enzymology; D015016:Yohimbine / Q000494:pharmacology; D000097564:Iodothyronine Deiodinase Type II
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D007453:Iodide Peroxidase; D011224:Prazosin; D011433:Propranolol; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D011943:Receptors, Adrenergic, beta; D013974:Thyroxine; D014284:Triiodothyronine; D015016:Yohimbine; D000097564:Iodothyronine Deiodinase Type II