Corticosterone enhances adrenocorticotropin-induced calcium signals in bovine adrenocortical cells

被引:8
作者
Chiyo, T
Yamazaki, T
Aoshika, K
Kominami, S
Ohta, Y [1 ]
机构
[1] Tokyo Univ Agr & Technol, Dept Biotechnol & Life Sci, Tokyo 1848588, Japan
[2] Hiroshima Univ, Fac Integrated Arts & Sci, Higashihiroshima 7398521, Japan
关键词
D O I
10.1210/en.2002-221126
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
The rapid effects of steroid hormones on Ca2+ signals have been examined in bovine adrenocortical cells. Among the steroid molecules tested, only corticosterone rapidly stimulated Ca2+ signals upon addition of ACTH, although corticosterone alone did not induce Ca2+ signals. Corticosterone also enhanced steroidogenesis induced by ACTH. The enhancement of ACTH-induced Ca2+ signals was also observed with membrane-impermeable corticosterone conjugated to BSA and was not inhibited by cycloheximide. In addition, corticosterone did not enhance Ca2+ signals induced by ATP or angiotensin II. These results suggest that corticosterone selectively stimulates ACTH-induced Ca2+ signals in a non-genomic way by acting on a target in the plasma membrane. Furthermore, the supernatants of cells incubated with ACTH or ATP enhanced Ca2+ signals, suggesting that steroids produced by such treatment act in an autocrine fashion. Consistent with this idea, these effects were inhibited by inhibitors of steroidogenesis (aminoglutethimide or metyrapone). These results show that steroid molecules synthesized in adrenocortical cells facilitate ACTH-induced Ca2+ signals. Taken together, corticosterone secreted from adrenocortical cells activates ACTH-induced Ca2+ signals and steroidogenesis by nongenomic means.
引用
收藏
页码:3376 / 3381
页数:6
相关论文
共 39 条
[1]
Characterization of specific corticosterone binding sites in adrenal cortex plasma membrane and their localization by autoradiographic studies [J].
Andres, M ;
Marino, A ;
Macarulla, JM ;
Trueba, M .
CELLULAR AND MOLECULAR LIFE SCIENCES, 1997, 53 (08) :673-680
[2]
The classical progesterone receptor associates with p42 MAPK and is involved in phosphatidylinositol 3-kinase signaling in Xenopus oocytes [J].
Bagowski, CP ;
Myers, JW ;
Ferrell, JE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (40) :37708-37714
[3]
Neurosteroids: A novel function of the brain [J].
Baulieu, EE .
PSYCHONEUROENDOCRINOLOGY, 1998, 23 (08) :963-987
[4]
Functional testosterone receptors in plasma membranes of T cells [J].
Benten, WPM ;
Lieberherr, M ;
Giese, G ;
Wrehlke, C ;
Stamm, O ;
Sekeris, CE ;
Mossmann, H ;
Wunderlich, F .
FASEB JOURNAL, 1999, 13 (01) :123-133
[5]
ANGIOTENSIN-II-STIMULATED CORTISOL SECRETION IS MEDIATED BY A HORMONE-SENSITIVE PHOSPHOLIPASE-C IN BOVINE ADRENAL FASCICULATA RETICULARIS CELLS [J].
BIRD, IM ;
MEIKLE, I ;
WILLIAMS, BC ;
WALKER, SW .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1989, 64 (01) :45-53
[6]
CHEITLIN R, 1985, J BIOL CHEM, V260, P5323
[7]
Submitochondrial distribution of three key steroidogenic proteins (steroidogenic acute regulatory protein and cytochrome p450(scc) and 3 beta-hydroxysteroid dehydrogenase isomerase enzymes) upon stimulation by intracellular calcium in adrenal glomerulosa cells [J].
Cherradi, N ;
Rossier, MF ;
Vallotton, MB ;
Timberg, R ;
Friedberg, I ;
Orly, J ;
Wang, XJ ;
Stocco, DM ;
Capponi, AM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (12) :7899-7907
[8]
A nongenomic mechanism for progesterone-mediated immunosuppression:: Inhibition of K+ channels, Ca2+ signaling, and gene expression in T lymphocytes [J].
Ehring, GR ;
Kerschbaum, HH ;
Eder, C ;
Neben, AL ;
Fanger, CM ;
Khoury, RM ;
Negulescu, P ;
Cahalan, MD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (09) :1593-1602
[9]
T-TYPE CA(2+) CHANNELS ARE REQUIRED FOR ADRENOCORTICOTROPIN-STIMULATED CORTISOL PRODUCTION BY BOVINE ADRENAL ZONA-FASCICULATA CELLS [J].
ENYEART, JJ ;
MLINAR, B ;
ENYEART, JA .
MOLECULAR ENDOCRINOLOGY, 1993, 7 (08) :1031-1040
[10]
A subset of kappa opioid ligands bind to the membrane glucocorticoid receptor in an amphibian brain [J].
Evans, SJ ;
Searcy, BT ;
Moore, FL .
ENDOCRINOLOGY, 2000, 141 (07) :2294-2300