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Thyroid Hormone (3,5,3'-Triido-L-Thyronine) Masking/Inversion of Stimulatory Effect of Androgen on Expression of mk1, a True Tissue Kallikrein, in the Mouse Submandibular Gland¹

Departments of Oral Physiology (K.K., T.U.), Dental Pharmacology (S.M., H.S.) and Biochemistry (N.N.), Meikai University School of Dentistry, Sakado, Saitama 350-0283, Japan

Address all correspondence and requests for reprints to: Kinji Kurihara Ph.D., Department of Oral Physiology, Meikai University School of Dentistry, 1–1 Keyaki-Dai, Sakado, Saitama 350-0283 Japan. E-mail: kkinji{at}dent.meikai.ac.jp

We studied hormonal regulation of the expression of mk1, a true tissue kallikrein, in the submandibular gland (SMG) of ICR, C3H/HeN, and F1 (mice from male C3H/HeN x female ICR and in the ones from male ICR x female C3H/HeN). In these mouse strains, mk1 was low in content in males, abundant in females, and increased remarkably by castration of males. In the case of ICR and both F1 mice, injection of 5-dihydrotestosterone (DHT) reduced the mk1 level of castrated and female mice. However, the mk1 content in female C3H/HeN mice (or castrated C3H/HeN) was further increased by DHT. To investigate the real action of DHT on mk1 expression, we examined the effects of adrenoectomy/glucocorticoid (dexamethasone, Dex) administration; DHT administration into castrated and adrenoectomized mice; ovariectomy/female hormone (17ß-estradiol, progesterone) administration; and hypophysectomy/combinatory administra-tion of DHT, Dex, and thyroid hormone (3,5,3'-triiodo-L-thyronine, T₃) on the mk1 expression in the SMG of ICR mice. Adrenoectomy or ovariectomy did not change the characteristic pattern of mk1 expression in male and female ICR mice. In hypophysectomized (Hypox) ICR male mice, the mk1 content was increased to the same level as in normal ICR females, and DHT administration into the Hypox mice further increased the mk1 level. However, combinatory administration of DHT + T₃ or of DHT + T₃ + Dex into the Hypox mice lowered the mk1 content to the level of normal ICR males, whereas T₃ single administration had no effect. Dex single administration into the Hypox mice increased the mk1 level to an even higher than that observed with DHT administration. The mk1 level in Hypox mice was not significantly changed by coadministration of Dex with T₃. From these results, we conclude that 1) mk1 expression is fundamentally stimulated by androgen (DHT) as are other mk isozymes, such as mk9, mk13, mk22, and mk26 in the mouse SMG, 2) the effect (stimulatory) of DHT on mk1 expression becomes, however, inverted (inhibitory) in the presence of T₃. Although the serum T₃ level of C3H/HeN female (0.52 ng/ml) was not significantly different from that of C3H/HeN males or ICR mice, coadministration of T₃ into C3H/HeN females with a fixed amount of DHT (20 mg/kg body weight) dose dependently repressed the DHT-induced increase in mk1 expression, suggesting the lower sensitivity of C3H/HeN females to T₃.

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				S. Kurabuchi, E. W. Gresik, and K. Hosoi Additive and/or Synergistic Action (Downregulation) of Androgens and Thyroid Hormones on the Cellular Distribution and Localization of a True Tissue Kallikrein, mK1, in the Mouse Submandibular Gland J. Histochem. Cytochem., November 1, 2004; 52(11): 1437 - 1446. [Abstract] [Full Text] [PDF]