PMID- 10803567
OWN - NLM
STAT- MEDLINE
DCOM- 20000523
LR  - 20161124
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 141
IP  - 5
DP  - 2000 May
TI  - Regulation by adrenocorticotropin (ACTH), angiotensin II, transforming growth 
      factor-beta, and insulin-like growth factor I of bovine adrenal cell 
      steroidogenic capacity and expression of ACTH receptor, steroidogenic acute 
      regulatory protein, cytochrome P450c17, and 3beta-hydroxysteroid dehydrogenase.
PG  - 1599-607
AB  - The purpose of this study was to evaluate the time-course effect of a 36-h 
      treatment with ACTH (10(-8) M), transforming growth factor-beta1 (TGFbeta1; 
      10(-10) M), angiotensin II (AngII; 10 (-7) M), and insulin-like growth factor I 
      (IGF-I; 10(-8) M) on the steroidogenic capacity of bovine adrenocortical cells 
      (BAC) and on messenger RNA (mRNA) levels of ACTH receptor, cytochrome P450c17, 
      3beta-hydroxysteroid dehydrogenase (3betaHSD), steroidogenic acute regulatory 
      protein (StAR), and StAR protein. ACTH and IGF-I enhanced, in a time-dependent 
      manner, the acute 2-h ACTH-induced cortisol production, whereas TGFbeta 1 and 
      AngII markedly reduced it. ACTH, IGF-I, and AngII increased ACTH receptor mRNA, 
      but the opposite was observed after TGFbeta1 treatment. ACTH and IGF-I increased 
      P450c17 and 3betaHSD mRNAs, whereas AngII and TGFbeta1 had the opposite effects. 
      However, the effects of the four peptides on ACTH-induced cortisol production 
      appeared before any significant alterations of the mRNA levels occurred. The most 
      marked and rapid effect of the four peptides was on StAR mRNA. The stimulatory 
      effect of ACTH was seen within 1.5 h, peaked at 4-6 h, and declined thereafter, 
      but at the end of the 36-h pretreatment, the levels of StAR mRNA and protein were 
      higher than those in control cells. IGF-I also enhanced StAR mRNA levels within 
      1.5 h, and these levels remained fairly constant. The effects of AngII on StAR 
      mRNA expression were biphasic, with a peak within 1.5-3 h, followed by a rapid 
      decline to almost undetectable levels of both mRNA and protein. TGFbeta1 had no 
      significant effect during the first 3 h, but thereafter StAR mRNA declined, and 
      at the end of the experiment the StAR mRNA and protein were almost undetectable. 
      Similar results were observed when cells were treated with ACTH plus TGFbeta1. A 
      2-h acute ACTH stimulation at the end of the 36-h pretreatment caused a higher 
      increase in StAR mRNA and protein in ACTH- or IGF-I-pretreated cells than in 
      control cells, which, in turn, had higher levels than cells pretreated with 
      TGFbeta1, ACTH plus TGFbeta1, or AngII. These results and the fact that the 
      stimulatory (IGF-I) or inhibitory (AngII and TGFbeta1) effects on ACTH-induced 
      cortisol production were more pronounced than those on the ability of cells to 
      transform pregnenolone into cortisol strongly suggest that regulation of StAR 
      expression is one of the main factors, but not the only one, involved in the 
      positive (IGF-I) or negative (TGFbeta1 and AngII) regulation of BAC for ACTH 
      steroidogenic responsiveness. A high correlation between steady state mRNA level 
      and acute ACTH-induced cortisol production favors this conclusion.
FAU - Le Roy, C
AU  - Le Roy C
AD  - INSERM, U-369, Institut Federatif Recherches en Endocrinologie de Lyon, France.
FAU - Li, J Y
AU  - Li JY
FAU - Stocco, D M
AU  - Stocco DM
FAU - Langlois, D
AU  - Langlois D
FAU - Saez, J M
AU  - Saez JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Phosphoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Corticotropin)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (steroidogenic acute regulatory protein)
RN  - 11128-99-7 (Angiotensin II)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - EC 1.1.- (3-Hydroxysteroid Dehydrogenases)
RN  - EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase)
SB  - IM
MH  - 3-Hydroxysteroid Dehydrogenases/*biosynthesis/genetics
MH  - Adrenal Cortex/*metabolism
MH  - Adrenocorticotropic Hormone/*physiology
MH  - Angiotensin II/*physiology
MH  - Animals
MH  - Cattle
MH  - Cells, Cultured
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Insulin-Like Growth Factor I/*physiology
MH  - Phosphoproteins/*biosynthesis/genetics
MH  - RNA, Messenger/metabolism
MH  - Receptors, Corticotropin/*biosynthesis/genetics
MH  - Steroid 17-alpha-Hydroxylase/*biosynthesis/genetics
MH  - Time Factors
MH  - Transforming Growth Factor beta/*physiology
EDAT- 2000/05/10 09:00
MHDA- 2000/06/08 09:00
CRDT- 2000/05/10 09:00
PHST- 2000/05/10 09:00 [pubmed]
PHST- 2000/06/08 09:00 [medline]
PHST- 2000/05/10 09:00 [entrez]
AID - 10.1210/endo.141.5.7457 [doi]
PST - ppublish
SO  - Endocrinology. 2000 May;141(5):1599-607. doi: 10.1210/endo.141.5.7457.