Glucocorticoid inhibits expression of V-1, a catecholamine biosynthesis regulatory protein, in cultured adrenal medullary cells

• Published in: FEBS letters Vol. 528; no. 1; pp. 166 - 170
• Main Authors: Hiwatashi, Yusuke, Kurahashi, Yusuke, Hatada, Risa, Ueno, Susumu, Honma, Takao, Yanagihara, Nobuyuki, Yanase, Haruko, Iwanaga, Toshihiko, Ohizumi, Yasushi, Yamakuni, Tohru
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 25.09.2002
• Subjects: Adrenal chromaffin cells; Adrenal Medulla - drug effects; Adrenal Medulla - metabolism; Animals; Catecholamine biosynthesis; Cells, Cultured; Chromaffin Cells - drug effects; Chromaffin Cells - metabolism; Dexamethasone - pharmacology; Dopamine beta-Hydroxylase - metabolism; Epinephrine - metabolism; Glucocorticoid; Glucocorticoids - pharmacology; Hormone Antagonists - pharmacology; Immunohistochemistry; Intercellular Signaling Peptides and Proteins; Mifepristone - pharmacology; Nerve Tissue Proteins - antagonists & inhibitors; Nerve Tissue Proteins - metabolism; Norepinephrine - metabolism; Rats; Rats, Wistar; Receptors, Glucocorticoid - antagonists & inhibitors; Tyrosine 3-Monooxygenase - metabolism; V-1 protein; Adrenal chromaffin cells; V-1 protein; Glucocorticoid; Catecholamine biosynthesis
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(02)03293-3

V-1 acts as a positive and coordinate regulator of gene expression of catecholamine biosynthetic enzymes in PC12D cells. The present study was conducted to investigate the mechanism controlling expression of V-1 in the adrenal gland. Immunohistochemical analysis demonstrated that noradrenergic chromaffin cells more highly expressed V-1 than adrenergic chromaffin cells preferentially expressing the glucocorticoid receptor in rat adrenal glands. Western blotting showed that in cultured bovine adrenal medullary cells, dexamethasone, a synthetic glucocorticoid, inhibited expression of V-1, and that this inhibition was prevented by RU-486, a glucocorticoid receptor antagonist. These results suggest that adrenal expression of V-1 is differentially controlled by glucocorticoids through the specific receptor, and that thereby V-1 regulates catecholamine biosynthesis in a catecholaminergic phenotype-dependent manner.